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Choledocholithiasis & Cholangitis
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Choledocholithiasis is the presence of stones in bile ducts; the stones can form in the gallbladder or in the ducts themselves. These stones cause biliary colic, biliary obstruction, gallstone pancreatitis, or cholangitis (bile duct infection and inflammation). Cholangitis, in turn, can lead to strictures, stasis, and choledocholithiasis. Diagnosis usually requires visualization by magnetic resonance cholangiopancreatography or ERCP. Early endoscopic or surgical decompression is indicated.

Stones may be described as:
• Primary stones (usually brown pigment stones), which form in the bile ducts
• Secondary stones (usually cholesterol), which form in the gallbladder but migrate to the bile ducts
• Residual stones, which are missed at the time of cholecystectomy (evident < 3 yr later)
• Recurrent stones, which develop in the ducts > 3 yr after surgery

In developed countries, > 85% of common duct stones are secondary; affected patients have additional stones located in the gallbladder. Up to 10% of patients with symptomatic gallstones also have associated common bile duct stones. After cholecystectomy, brown pigment stones may result from stasis (eg, due to a postoperative stricture) and the subsequent infection. The proportion of ductal stones that are pigmented increases with time after cholecystectomy.

Bile duct stones may pass into the duodenum asymptomatically. Biliary colic occurs when the ducts become partially obstructed. More complete obstruction causes duct dilation, jaundice, and, eventually, cholangitis (a bacterial infection). Stones that obstruct the ampulla of Vater can cause gallstone pancreatitis. Some patients (usually the elderly) present with biliary obstruction due to stones that have caused no symptoms previously.

In acute cholangitis, bile duct obstruction allows bacteria to ascend from the duodenum. Most (85%) cases result from common bile duct stones, but bile duct obstruction can result from tumors or other conditions. Common infecting organisms include gram-negative bacteria (eg, Escherichia coli , Klebsiella sp, Enterobacter sp); less common are gram-positive bacteria (eg, Enterococcus sp) and mixed anaerobes (eg, Bacteroides sp, Clostridia sp). 

Symptoms include:

RUQ abdominal pain, jaundice, and fever or chills (Charcot triad)

The abdomen is tender, and often the liver is tender and enlarged (often containing abscesses). Confusion and hypotension predict about a 50% mortality rate and high morbidity.

• Liver function tests
• Ultrasonography

Common duct stones should be suspected in patients with jaundice and biliary colic. Fever and leukocytosis further suggest acute cholangitis. Elevated levels of bilirubin and particularly alkaline phosphatase, ALT, and γ-glutamyltransferase are consistent with extrahepatic obstruction, suggesting stones, particularly in patients with features of acute cholecystitis or cholangitis.

Ultrasonography may show stones in the gallbladder and occasionally in the common duct (less accurate). The common duct is dilated (> 6 mm in diameter if the gallbladder is intact; > 10 mm after a cholecystectomy). If the ducts are not dilated early in the presentation (eg, first day), stones have probably passed. If doubt exists, magnetic resonance cholangiopancreatography (MRCP) is highly accurate for retained stones. ERCP is done if MRCP is equivocal; it can be therapeutic as well as diagnostic. CT, though less accurate than ultrasonography, can detect liver abscesses.

For suspected acute cholangitis, CBC and blood cultures are essential. Leukocytosis is common, and aminotransferases may reach 1000 IU/L, suggesting acute hepatic necrosis, often due to microabscesses. Blood cultures guide antibiotic choice.

• ERCP and sphincterotomy

If biliary obstruction is suspected, ERCP and sphincterotomy are necessary to remove the stones. Success rate exceeds 90%; up to 7% of patients have short-term complications (eg, bleeding, pancreatitis, infection). Long-term complications (eg, stone recurrence, fibrosis and subsequent duct stricture) are more common. Laparoscopic cholecystectomy, which is not as well-suited for operative cholangiography or common duct exploration, can be done electively after ERCP and sphincterotomy. Mortality and morbidity after open cholecystectomy with common duct exploration are higher. In patients at high risk of complications with cholecystectomy (eg, the elderly), sphincterotomy alone is an alternative.

Acute cholangitis is an emergency requiring aggressive supportive care and urgent removal of the stones, endoscopically or surgically. Antibiotics are given, similar to those used for acute cholecystitis. An alternative regimen for very ill patients is imipenem and ciprofloxacin plus metronidazole to cover anaerobes.

Key Points
• In developed countries, > 85% of common duct stones form in the gallbladder and migrate to the bile ducts; most are cholesterol stones.
• Suspect common duct stones if patients have biliary colic, unexplained jaundice, and/or elevated, alkaline phosphatase, and γ-glutamyltransferase levels.
• Do ultrasonography and, if inconclusive, MRCP.
• Do ERCP and sphincterotomy to remove a stone that causes obstruction.
• For acute cholangitis, remove stones as soon as possible and give antibiotics.


A 64-year-old woman presents to the emergency department with abdominal pain and fever. She has had a long history of mild, intermittent dyspepsia that frequently has followed meals. She has had diabetes for 12 years, and although her response to oral hypoglycemic agents has been poor, she has refused to use insulin. At the time of presentation, she has been ill for 36 hours with vomiting, fever, and abdominal pain. On examination, she is febrile with a temperature of 38.9􏰁C and has tachycardia of 124 bpm. She is mildly jaundiced. Bowel sounds are diminished, and tenderness and guarding are most marked in the right upper quadrant. Toward the end of the examination, rigor is evident, and she has broken into a sweat. Which of the following is most likely to be her problem?

A. Pancreatitis with abscess
B. Cholangitis
C. Perforated peptic ulcer
D. Splenic abscess
E. Esophageal reflux

The answer is B. According to the patient, she has certainly had cholecystitis in the past. With gallstones in the gallbladder, there is always some risk of migration to the common bile duct and subsequent obstruction of the duct. The infection that may follow obstruction of the common bile duct may be very serious, with bacteremia and sepsis as common sequelae. Pancreatic abscess can manifest as abdominal pain, but it does not have the associated localized right upper quadrant findings as often as cholangitis. Perforated ulcers lead to peritonitis. Splenic abscesses are almost always the sequelae of bacteremia (e.g., with endocarditis). Reflux esophagitis can cause severe heartburn but does not result in sepsis.

A 36-year-old woman comes to the office because of a 3-day history of "yellow skin," fever, and abdominal pain. The pain is mostly present in the right upper quadrant. However she sometimes feels it in her right shoulder. She has had several similar episodes in the past, but they were not accompanied by fever, and skin discoloration. She is married & has 3 children, none of whom are sick. Her temperature is 39.3 C (102.7 F), blood pressure is 110/70 mm Hg, pulse is 70/min, and respirations are 20/min. Physical examination shows right upper quadrant tenderness. She has the "chills", but she continues to breathe normally during right upper quadrant palpation. Lab studies show ALT 109 U/L, AST 90 U/L, Total Bilirubin 4.9 mg/dL, direct Bilirubin 3.8 mg/dL.
The most likely diagnosis is

A. acute cholangitis
B. acute cholecystitis
C. acute hepatitis
D. acute pancreatitis
E. biliary colic

The correct answer is A. This patient has fever, jaundice, and right upper quadrant abdominal pain, Charcot's triad, which is usually diagnostic of acute cholangitis. This typically occurs because of a stone impacted within the common bile duct. Blockage of this duct results in cholestatic jaundice, hence the elevated bilirubin, and high alkaline phosphatase. Gram-negative bacteria penetrate into the biliary ducts, and cause inflammation with leukocytosis and fever. The pain is due to gallbladder distention. The treatment involves antibiotics and surgery.

Acute cholecystitis (choice B), is inflammation of the gallbladder and the obstruction of the cystic duct by a gallstone. Symptoms include right upper quadrant pain, a mild fever, and possibly nausea and vomiting. Physical examination shows right upper quadrant pain with inspiratory arrest during palpation, (Murphy's sign). Mild jaundice may occur. The leukocyte count is elevated. Treatment includes antibiotics and surgery.

Acute hepatitis (choice C), manifests with mild right upper quadrant abdominal pain, nausea, anorexia, and a low-grade fever. Serum alanine aminotransferase and aspartate aminotransferase are markedly elevated, helping to distinguish this from cholangitis.

Acute pancreatitis (choice D), typically presents with intense midepigastric pain, usually radiating to the back, fever, nausea, and vomiting. Very high levels of amylase and lipase will support the diagnosis. The treatment usually involves insertion of a nasogastric tube, intravenous fluids, and electrolyte replacement.

Biliary colic (choice E), is episodic right upper quadrant abdominal pain that radiates to the back, and may be associated with nausea and vomiting. It often occurs after a meal. It is caused by a transient blockage of the cystic duct with a gallstone. It is not usually associated with fever or jaundice.

A 38-year-old woman comes to the emergency room complaining of severe, right-sided abdominal pain, fever, and chills for the past several hours. She has a history of gallstones and her family doctor recommended a cholecystectomy after a similar episode several months ago. Upon examination, she has a temperature of 102.7°F (39.3°C), is tender in the right upper quadrant, and is visibly jaundiced. Her white blood count is 18,000/mm3 .In which of the following locations is a gallstone most likely lodged in this patient?

A. Common bile duct
B. Cystic duct
C. Fundus of gallbladder
D. Proximal duodenum
E. Terminal ileum

The correct answer is A. The patient is probably suffering from choledocholithiasis, a condition in which a gallstone becomes lodged in the common bile duct. She is displaying "Charcot's triad" (fever, jaundice, and right upper quadrant pain), which is indicative of cholangitis (infection of the biliary tree proximal to an obstruction such as a gallstone or malignancy). Gallstones are very common, occurring in as many as 15-20% of the general population. The most common type of stone contains cholesterol, which precipitates from supersaturated bile within the gallbladder. Some risk factors for cholesterol stones are increasing age, rapid weight loss, oral contraceptive use, and either disease of or resection of the terminal ileum (the site at which bile salts are reabsorbed). Pigmented gallstones made of calcium bilirubinate are less common and occur in patients with hemolytic disorders and certain types of biliary tract infections.

The key point in this case is the fact that the patient is jaundiced, eliminating all choices other than a stone in the common bile duct. Stones within the cystic duct (choice B) or gallbladder (choice C) do not cause jaundice. A stone within the small intestine (choices D and E) could cause jaundice only if it were very large and physically obstructing the biliary tree from within the intestinal lumen, which would be very unlikely.
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Renal Artery Stenosis
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Renal artery stenosis is a decrease in blood flow through one or both of the main renal arteries or their branches. Renal artery occlusion is a complete blockage of blood flow through one or both of the main renal arteries or its branches. Stenosis and occlusion are usually due to thromboemboli, atherosclerosis, or fibromuscular dysplasia. Symptoms of acute occlusion include steady, aching flank pain, abdominal pain, fever, nausea, vomiting, and hematuria. Acute kidney injury may develop. Chronic, progressive stenosis causes refractory hypertension and may lead to chronic kidney disease. Diagnosis is by imaging tests (eg, CT angiography, magnetic resonance angiography). Treatment of acute occlusion is with anticoagulation and sometimes fibrinolytics and surgical or catheter-based embolectomy, or a combination. Treatment of chronic, progressive stenosis includes angioplasty with stenting, surgical bypass, and removal of an infarcted kidney.

Renal hypoperfusion results in hypertension, renal failure, and, if complete occlusion occurs, renal infarction and necrosis.


Occlusion may be acute or chronic. Acute occlusion is usually unilateral. Chronic occlusion may be unilateral or bilateral.

Acute renal artery occlusion

The most common cause is thromboembolism. Emboli may originate in the heart (due to atrial fibrillation, after MI, or from vegetations due to bacterial endocarditis) or the aorta (as atheroemboli); less often, fat or tumor emboli are the cause. Thrombosis may occur in a renal artery spontaneously or after trauma, surgery, angiography, or angioplasty. Other causes of acute occlusion include dissection or rupture of a renal artery aneurysm.

Rapid, total occlusion of large renal arteries for 30 to 60 min results in infarction. The infarct is typically wedge-shaped, radiating outward from the affected vessel.

Chronic progressive renal artery stenosis

About 90% of cases are due to atherosclerosis, which is usually bilateral. Almost 10% of cases are due to fibromuscular dysplasia (FMD), which is commonly unilateral. Less than 1% of cases result from Takayasu arteritis, Kawasaki disease, neurofibromatosis type 1, aortic wall hematoma, or aortic dissection.

Atherosclerosis develops primarily in patients > 50 (more often men) and usually affects the aortic orifice or proximal segment of the renal artery. Chronic progressive stenosis tends to become clinically evident after about 10 yr of atherosclerosis, causing renal atrophy and chronic kidney disease.

FMD is pathologic thickening of the arterial wall, most often of the distal main renal artery or the intrarenal branches. The thickening tends to be irregular and can involve any layer (but most often the media). This disorder develops primarily in younger adults, particularly in women aged 20 to 50. It is more common among 1st-degree relatives of patients with FMD and among people with the ACE1 gene.

Symptoms and Signs

Manifestations depend on rapidity of onset, extent, whether unilateral or bilateral, and duration of renal hypoperfusion. Stenosis of one renal artery is often asymptomatic for a considerable time.

Acute complete occlusion of one or both renal arteries causes steady and aching flank pain, abdominal pain, fever, nausea, and vomiting. Gross hematuria, oliguria, or anuria may occur; hypertension is rare. After 24 h, symptoms and signs of acute kidney injury may develop. If the cause was thromboembolic, features of thromboembolism at other sites (eg, blue toes, livedo reticularis, retinal lesions on funduscopic examination) also may be present.

Chronic progressive stenosis causes hypertension, which may begin at an atypical age (eg, < 30 yr or after age 50 yr) and which may be refractory to control despite use of multiple antihypertensives. Physical examination may detect an abdominal bruit or signs of atherosclerosis. Symptoms and signs of chronic kidney disease develop slowly.

• Clinical suspicion
• Imaging

Diagnosis is suspected in patients with renal failure and who have

• Symptoms of acute renal artery occlusion
• Symptoms or signs of thromboembolism

Hypertension that begins before age 30 or is refractory to treatment with > 3 antihypertensive drugs

Blood and urine tests are done to confirm renal failure. Diagnosis is confirmed by imaging tests. Which tests are done depends on the patient’s renal function and other characteristics and on test availability.

Some tests (CT angiography, arteriography, digital subtraction angiography) require an IV ionic radiocontrast agent, which may be nephrotoxic; this risk is lower with the nonionic hypo-osmolar or iso-osmolar contrast agents that are now in widespread use. Magnetic resonance angiography (MRA) requires the use of gadolinium contrast; in patients with severe chronic kidney disease, gadolinium contrast carries the risk of nephrogenic systemic fibrosis, a condition that closely resembles systemic sclerosis and that has no satisfactory method of treatment.

When results of other tests are inconclusive or negative but clinical suspicion is strong, arteriography is necessary for definitive diagnosis. Arteriography may also be needed before invasive interventions.

When a thromboembolic disorder is suspected, ECG (to detect atrial fibrillation) and hypercoagulability studies may be needed to identify treatable embolic sources. Transesophageal echocardiography is done to detect atheromatous lesions in the ascending and thoracic aorta and cardiac sources of thrombi or valvular vegetations.

Blood and urine tests are nondiagnostic but are done to confirm renal failure, indicated by elevated creatinine and BUN and by hyperkalemia. Leukocytosis, gross or microscopic hematuria, and proteinuria may also be present.


Acute renal artery occlusion

A renal thromboembolic disorder may be treated with a combination of anticoagulation, fibrinolytics, and surgical or catheter-based embolectomy. Treatment within 3 h of symptom onset is likely to improve renal function. However, complete recovery is unusual, and early and late mortality rates are high because of extrarenal embolization or underlying atherosclerotic heart disease.

Patients presenting within 3 h may benefit from fibrinolytic (thrombolytic) therapy (eg, streptokinase, alteplase) given IV or by local intra-arterial infusion. However, such rapid diagnosis and treatment are rare.

All patients with a thromboembolic disorder require anticoagulation with IV heparin, unless contraindicated. Long-term anticoagulation with oral warfarin can be initiated simultaneously with heparin if no invasive intervention is planned. Anticoagulation should be continued for at least 6 to 12 mo—indefinitely for patients with a recurrent thromboembolic disorder or a hypercoagulability disorder.

Surgery to restore vascular patency has a higher mortality rate than fibrinolytic therapy and has no advantage in recovery of renal function. However, surgery, particularly if done within the first few hours, is preferred for patients with traumatic renal artery thrombosis. If patients with nontraumatic, severe renal failure do not recover function after 4 to 6 wk of drug therapy, surgical revascularization (embolectomy) can be considered, but it helps only a few.

If the cause is thromboemboli, the source should be identified and treated appropriately.

Chronic progressive renal artery stenosis

Treatment is indicated for patients who meet one or more of the following 5 criteria:

• Hypertension refractory to medical treatment with ≥ 3 drugs
• Deterioration of renal function despite optimal medical therapy
• A short duration of BP elevation prior to the diagnosis of renovascular disease
• Recurrent flash pulmonary edema
• Unexplained rapid progression of renal insufficiency

Treatment is with percutaneous transluminal angioplasty (PTA) plus stent placement or with surgical bypass of the stenotic segment. Usually, an extensively infarcted kidney must be removed if revascularization is not expected to result in functional recovery. Surgery is usually more effective than PTA for atherosclerotic occlusion; it cures or attenuates hypertension in 60 to 70% of patients. However, surgery is considered only if patients have complex anatomic lesions or if PTA is unsuccessful, particularly with repeated in-stent restenosis. PTA is preferred for FMD; risk is minimal, success rate is high, and restenosis rate is low.

Renovascular hypertension

Treatments are typically ineffective unless vascular patency is restored. ACE inhibitors, angiotensin II receptor blockers, or renin inhibitors can be used in unilateral and, if GFR is monitored closely, in bilateral renal artery stenosis. These drugs can reduce GFR and increase serum BUN and creatinine levels. If GFR decreases enough to increase serum creatinine, Ca channel blockers (eg, amlodipine, felodipine) or vasodilators (eg, hydralazine, minoxidil) should be added or substituted.

Key Points
• Renal artery stenosis or occlusion may be acute (usually due to thromboembolism) or chronic (usually due to atherosclerosis or fibromuscular dysplasia).
• Suspect acute occlusion if patients have steady, aching flank or abdominal pain, and sometimes fever, nausea and vomiting, and/or gross hematuria.
• Suspect chronic occlusion in patients who develop unexplained severe or early-onset hypertension.
• Confirm the diagnosis with vascular imaging.
• Restore vascular patency for patients who have acute occlusion and for selected patients (eg, with severe complications or refractory disease) who have chronic occlusion.
• Hypertension is difficult to control until vascular patency is restored, but begin treatment with ACE inhibitors, angiotensin II receptor blockers, or renin inhibitors; closely monitor GFR; and substitute Ca channel blockers or vasodilators if GFR decreases.


A 67-year-old man who had been successfully medicated for hypertension for the past 15 years develops a diastolic pressure of 110 mm Hg. At that time, he was taking hydrochlorothiazide, acebutolol, clonidine, and doxazosin mesylate for his blood pressure and metformin for type 2 diabetes. A serum panel was unremarkable, except that his creatinine level was 4 mg/dL (normal, 0.6–1.2 mg/dL), and his blood urea nitrogen (BUN) was 28 mg/dL (normal, 8–20 mg/dL). In an attempt to lower his blood pressure, his physician added enalapril; the patient rapidly developed renal failure. Which of the following choices represents the most likely diagnosis?

A. Renal arterial stenosis due to fibromuscular dysplasia
B. Acute renal artery occlusion
C. Renal vein thrombosis due to a malignant occlusion
D. Malignant hypertension
E. Renal arterial stenosis due to occlusive arteriosclerotic disease

The answer is E. In the general population, fewer than 5% of the cases of hypertension result from renal arterial occlusion. However, renovascular occlusion accounts for 70% of the cases of hypertension in patients over the age of 60 who have a diastolic blood pressure above 105 mm Hg and a serum creatine value above 2 mg/dL; moreover 80% to 90% of these cases are due to occlusive arteriosclerotic disease (choice E). If both kidneys are occluded, provision of an angiotensin-converting enzyme (ACE) inhibitor, such as enalapril, tends to provoke acute renal failure because the ACE inhibitor decreases angiotensin II production, which is required for effective renal circulation. This is noted on renal function tests by a rising creatinine level.

About 10% to 15% of the cases of renal arterial stenosis are due to fibromuscular dysplasia (choice A); renal stenosis is almost unique among the renal diseases in that it is not accompanied by proteinuria, since the glomerulus is intact and renal arterial pressure is decreased. However, these cases primarily occur in females who are between the ages of 30 and 50 years. Renal vein thrombosis due to a malignant occlusion (choice C) presents with severe back pain and hyperproteinuria. Symptoms of malignant hypertension (choice D) include rapid and extreme increase in systolic blood pressure (over 200 mm Hg), blurred vision, headache, shortness of breath, chest pain, proteinuria, and sometimes seizures. Such an acute attack occa- sionally occurs for no apparent reason, usually in a person who was being treated for hypertension. It is the extreme increase in systolic pressure that induces the other symptoms, which will get worse the longer the pressure remains elevated. Consequently, this is a medical emergency; the pressure must be reduced imme- diately, usually by IV administration of antihypertensive agents.

Even though an arthrosclerotic artery is more readily occluded than a healthy one, by definition acute renal artery occlusion (choice B) differs from occlusion due to stenosis in that the latter is a chronic event. However, other difference between an acute occlusion and an occlusion due to stenosis are that the acute occlusion generally is unilateral, whereas stenosis is bilateral 70% of the time, and acute occlusion presents with backache and blood in the urine, whereas stenosis presents with hypertension. An occlusion generally occurs after major surgery or trauma affecting the abdomen or side or in individuals with atrial fibrillation or mitral or valve disease.

A 21-year-old man has been found to be hypertensive with bilateral arm blood pressures in the 140-160/100-110 mm Hg range on several visits. The patient has no past medical history and has no complaints. Review of systems is significant for occasional “band-like headaches". Physical examination is normal including a normal retinal examination. Urinalysis is normal. An electrocardiogram demonstrates normal sinus rhythms at a rate of 75/min, with mild left ventricular hypertrophy. His blood pressure is now 150/100 mm Hg after treatment with maximal doses of atenolol, hydrochlorothiazide, and captopril. The next step in the evaluation of this patient's hypertension is to

A. order a duplex ultrasound of the renal arteries
B. order an echocardiogram
C. prescribe triamterene
D. repeat the electrocardiogram

The correct answer is A. This patient should be suspected of having renal artery stenosis, most likely secondary to fibromuscular dysplasia from the early age of onset of severe hypertension. In addition, the poor control of this patient's hypertension, even with three agents is suspicious for renovascular hypertension. About 5% of patients with hypertension have renovascular hypertension. The renal arteries need to be evaluated by duplex ultrasound of the renal arteries, conventional angiography, spiral computed tomography, or magnetic resonance angiography.

Given signs of left ventricular hypertrophy on electrocardiogram, echocardiography (choice B) is warranted. The next immediate step however, is an evaluation of the renal arteries.

Triamterene (choice C) is a potassium-sparing diuretic often used in conjunction with hydrochlorothiazide. It is very unlikely that the three agents prescribed in high doses could not control the blood pressure of a patient with essential hypertension. Renovascular hypertension must be suspected.

Repeat electrocardiograms (choice D) should be performed every year to evaluate for the development of end-organ damage in a chronic hypertensive. This patient has electrocardiographic evidence of left ventricular hypertrophy. However, it is best followed with echocardiography.

A 29-year-old woman has become hypertensive and BP levels are difficult to control. You have her on 10 mg lisinopril twice daily, hydrochlorthiazide/triamterene once daily, and 80 mg verapamil 3 times daily. BP levels run 160/105 despite the foregoing. Serum potassium was normal before therapy was started. The 24-hour urine studies for VMA, metanephrine, and free catecholamines were within normal limits. Which of the following may be helpful in further elucidating the diagnosis?

B. Liver function profile 
C. Lipid screen
D. Abdominal examination 
E. Complete blood count

The answer is D. The patient should be examined for an abdominal bruit, specifically a bruit deep in one flank that could be generated by renal artery stenosis. Essential hypertension, be it volume dependent or based more on peripheral vascular resistance, usually has its clinical onset in a person’s late 30s or 40s. Hypertension significantly earlier or that which comes on after a person reaches the age of 60 must be evaluated for other causes, of which renovascular type is one. When a person is at a younger age, the cause is most likely due to a congenital fibrous band, which has a 2:1 female-to-male occurrence ratio. After a person reaches the age of 60, the cause is more likely an atherosclerotic one, which has a 2:1 male-to- female occurrence ratio. None of the other choices has any specific relevance to the diagnosis of the pathophysiology of hypertension.
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Erythema Infectiosum
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Erythema infectiosum, acute infection with parvovirus B19, causes mild constitutional symptoms and a blotchy or maculopapular rash beginning on the cheeks and spreading primarily to exposed extremities. Diagnosis is clinical, and treatment is generally not needed.

The disease is caused by human parvovirus B19. It occurs mostly during the spring, commonly causing localized outbreaks every few years among children (particularly children aged 5 to 7 yr). Spread seems to be by respiratory droplets and by percutaneous exposure to blood or blood products, with high rates of secondary infection among household contacts; infection can occur without symptoms or signs.


Parvovirus B19 causes transient suppression of erythropoiesis that is mild and asymptomatic except in children with underlying hemoglobinopathies (eg, sickle cell disease) or other RBC disorders (eg, hereditary spherocytosis), who may develop transient aplastic crisis. Also, immunocompromised children can develop protracted viremia (lasting weeks to months), leading to severe anemia (pure RBC aplasia).

Erythema infectiosum can be transmitted transplacentally, sometimes resulting in stillbirth or severe fetal anemia with widespread edema (hydrops fetalis). However, about half of pregnant women are immune because of previous infection. The risk of fetal death is 2 to 6% after maternal infection, with risk greatest during the first half of pregnancy.

Symptoms and Signs

The incubation period is 4 to 14 days. Typical initial manifestations are nonspecific flu-like symptoms (eg, low-grade fever, slight malaise). Several days later, an indurated, confluent erythema appears over the cheeks (“slapped-cheek” appearance) and a symmetric rash appears that is most prominent on the arms, legs (often extensor surfaces), and trunk, usually sparing the palms and soles. The rash is maculopapular, tending toward confluence; it forms reticular or lacy patterns of slightly raised, blotchy areas with central clearing, usually most prominent on exposed areas. The rash, and the entire illness, typically lasts 5 to 10 days. However, the rash may recur for several weeks, exacerbated by sunlight, exercise, heat, fever, or emotional stress.

Mild joint pain and swelling (nonerosive arthritis) that may persist or recur for weeks to months sometimes occurs in adults. A few patients (more commonly children) develop papular-purpuric gloves-and-socks syndrome (PPGSS), which causes papular, purpuric, or petechial lesions limited to the hands and feet and is often accompanied by fever and oral and/or genital lesions.


• Clinical evaluation

The appearance and pattern of spread of the rash are the only diagnostic features; however, some enteroviruses may cause similar rashes. Rubella can be ruled out by serologic testing; an exposure history is also helpful. Serologic testing is not required in otherwise healthy children; however, children with a known hemoglobinopathy or immunocompromised state should have CBC and reticulocyte count to detect hematopoietic suppression as well as viral testing. In children with transient aplastic crisis or adults with arthropathy, the presence of IgM-specific antibody to parvovirus B19 in the late acute or early convalescent phase strongly supports the diagnosis. Parvovirus B19 viremia also can be detected by quantitative PCR techniques, which are generally used for patients with transient aplastic crisis, immunocompromised patients with pure RBC aplasia, and infants with hydrops fetalis or congenital infection.


• Supportive care

Only symptomatic treatment is needed. IV immune globulin has been used to curtail viremia and increase erythropoiesis in immunocompromised patients with pure RBC aplasia.

Key Points
• Children develop low-grade fever and slight malaise followed several days later by an indurated, confluent erythema on the cheeks (“slapped-cheek” appearance) and a symmetric rash that is most prominent on the arms, legs, and trunk.
• There is mild, transient suppression of erythropoiesis that is asymptomatic except sometimes in children with hemoglobinopathies (eg, sickle cell disease) or other RBC disorders (eg, hereditary spherocytosis), or immunosuppression.
• Risk of fetal death is 2 to 6% after maternal infection.
• Testing is done mainly in children with transient aplastic crisis or adults with arthropathy.
• Treatment is symptomatic, but immunocompromised children may benefit from IV immune globulin.


A 4-year-old otherwise healthy boy is brought to the family physician’s office with an 8-day history of non- specific malaise and low grade fever as he begins to feel better now manifests a red maculopapular rash on the cheeks that on the day he is brought in appears to be coalescing to produce a diffuse red color now involving the chin and area behind the ears as well as the trunk and buttocks, sparing the circumoral zone. There is no palpable lymphadenopathy and the oral examination is not remarkable for descriptive abnormality. Which of the following is the likely diagnosis?

A. Rubella
B. Rubeola
C. Erythema infectiosum
D. Roseola infantum subitum 
E. Atopic dermatitis

The answer is C. Erythema infectiosum or fifth dis- ease. The “slapped cheek” look is like none of the other choices. Rubella has a much shorter course, a typical morbilliform rash and suboccipital and post auricular adenopathy. Rubeola manifest a seriously toxic illness, the harder and more severe morbilliform rash and the buccal mucosal Koplik spots opposite the lower second molar; roseola is the well-known rash that appears as a prolonged highly febrile phase abates.

A 6-year-old girl is brought to the clinic because of a 24-hour history of an "itchy, red rash." Over the past 7 days she has not been feeling well. She had a fever reaching 39.3 C (102.8 F), a headache, and muscle aches. Her mother treated her with acetaminophen and these symptoms resolved. Now she has this rash that appeared over night, as the other symptoms resolved. Her temperature is 37 C (98.6 F). Physical examination shows an erythematous facial rash on the cheeks and a symmetric, maculopapular, lace-like rash on the arms, buttocks, and thighs. The remainder of the examination is unremarkable. Laboratory studies show:

Leukocyte  36.000/mm3
Platelet    350,000/mm3

At this time the most correct statement about her condition is:

A. Droplet precautions should be used to prevent the spread of infection
B. Intravenous immunoglobulin therapy should be given
C. Pregnant women should not have contact with this patient
D. She should return to school after this office visit
E. She should be given a blood transfusion to prevent an aplastic crisis

The correct answer is D. This patient has the classic symptoms of an erythema infectiosum (fifth disease), which is an infection caused by Parvovirus B19. Patients with this disease are only infectious before the onset of the rash, during the period with the nonspecific febrile illness. The virus typically only causes a significant, severe illness in individuals with sickle cell disease and other hemoglobinopathies. In rare cases, has parvovirus, during pregnancy, been associated with fetal hydrops and death. But as stated earlier, this patient can go back to school because she is no longer contagious.

Droplet precautions used to prevent the spread of infection (choice A), is unnecessary at this stage in the disease because this patient is no longer infectious. Droplet precautions are used in hospitals for those caring for patients with diseases that are transmitted through droplets containing microorganisms. They are used to prevent the host from catching the infection if the infected patient coughs or sneezes on them or during procedures such as suctioning or bronchoscopy. Droplet precautions require a mask if within 3 feet of the patient and or in a private room. In addition to standard precautions, parvovirus B19 requires droplet precautions for those caring for these hospitalized patients.

Intravenous immunoglobulin therapy (choice B) is given to immunocompromised patients with chronic parvovirus infection. Supportive care is all that is indicated for this patient.

Since this patient is no longer infectious, it is incorrect to say that pregnant women should not have contact with this patient (choice C).

Parvovirus B19 is associated with thrombocytopenia, neutropenia, and red blood cell aplasia usually in patients with sickle cell disease and other hemoglobinopathies. Transfusions are used in these patients with aplastic crises. Transfusions are not routinely given in previously healthy children who have parvovirus B19 infection to prevent aplastic crises. Since this patient's complete blood count is normal, she should NOT be given a blood transfusion to prevent an aplastic crisis (choice E).

You care for a 32-year-old school teacher who is in the second half of her pregnancy. A 6-year-old boy came to class on the first day of school with "an infection with 'slapped cheeks' and a lace-like rash." His mother told your patient that the boy became sick with a high fever, muscle aches, and a headache 10 days before school started. When these symptoms subsided, this rash suddenly appeared 1 day ago. A doctor examined the boy and told the mother that all of his "blood work" was normal. Since this boy did not want to miss the first day of classes and he "felt fine" his mother allowed him to attend school. Even though your patient is asymptomatic, she is worried about her health and the health of her unborn baby. The best next step is to

A. administer intravenous immunoglobulin therapy to prevent infection
B. advise her to have an amniocentesis to evaluate the unborn baby's health
C. advise her to stay home from school until the boy's rash disappears
D. ask her to return for reexamination in 1 week
E. reassure her of the relatively low potential risk to her and her unborn baby

The correct answer is E. The boy in this patient's class has the classic symptoms of erythema infectiosum (Fifth disease), which is an infection caused by Parvovirus B19. Patients with this disease are only infectious before the onset of the rash, during the period with the nonspecific febrile illness. The virus typically only causes a significant, severe illness in individuals with sickle cell disease and other hemoglobinopathies. In rare cases, parvovirus contracted during pregnancy has been associated with fetal hydrops and death. But as stated earlier, the boy in this pregnant patient's class was contagious before school started, and since he is no longer contagious, she should be reassured of the relatively low potential risk to her and her unborn baby. If she was in contact with him during the phase of the illness before the onset of the rash, she should have serologic testing and a fetal ultrasound to evaluate the health of her and the baby. It should be mentioned that the complications of parvovirus in pregnant women typically occur during the first half of pregnancy.

It is inappropriate to administer intravenous immunoglobulin therapy to prevent infection (choice A) because the boy that this patient was in contact with, was most likely no longer contagious. Intravenous immunoglobulin therapy is given to immunocompromised patients with chronic parvovirus infection. Supportive care is all that is indicated for patients with a typical parvovirus B19 infection. The patient in this case does not require any preventive treatment.

Since this patient was not exposed to the boy in the contagious phase of the disease, it is inappropriate to advise her to have an amniocentesis to evaluate the unborn baby's health (choice B). Also, since the greatest risk to the unborn baby is during the first half of the pregnancy, she should be reassured of the low risk of complications.

It is incorrect to advise her to stay home from school until the boy's rash disappears (choice C) because the boy in her class in no longer infectious.

It is unnecessary to ask her to return for reexamination in 1 week (choice D) because the boy in her class is no longer contagious and so it is unlikely that she will develop symptoms. However, it is appropriate to advise her to come back to the office if she does develop any symptoms.
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Psoriasis is an inflammatory disease that manifests most commonly as well-circumscribed, erythematous papules and plaques covered with silvery scales. Multiple factors contribute, including genetics. Common triggers include trauma, infection, and certain drugs. Symptoms are usually minimal, but mild to severe itching may occur. Cosmetic implications may be major. Some people develop severe disease with painful arthritis. Diagnosis is based on appearance and distribution of lesions. Treatment can include emollients, vitamin D analogs, topical retinoids, tar, anthralin, corticosteroids, phototherapy, and, when severe, methotrexate, oral retinoids, immunomodulatory agents (biologics), or immunosuppressants.

Psoriasis is hyperproliferation of epidermal keratinocytes combined with inflammation of the epidermis and dermis. It affects about 1 to 5% of the population worldwide; light-skinned people are at higher risk, and blacks are at lower risk. Peak onset is roughly bimodal, most often at ages 16 to 22 and at ages 57 to 60, but the disorder can occur at any age.

Psoriasis is a chronic, relapsing skin disease that manifests as a papulosquamous eruption with variable clinical manifestations but typically occurs as inflammatory plaques with excessive white scaling in a predominately extensor distribution.

Etiology of Psoriasis

Psoriasis appears to be an autoimmune disease with a genetic predisposition. It is mostly likely inherited as a polygenic, autosomal dominant disease with variable penetrance. The precise target of the immune response is unknown. HLA-B13, HLA-B17, HLA-BW57, and HLA-CW6 are most frequently associated with psoriasis. As many as one third of patients report that one family member is affected. Psoriasis tends to flare during winter months and improve in the summer months as a function of sun (UV) exposure. Drugs that exacerbate psoriasis include 􏰄-adrenergic blockers, lithium, and angiotensin-converting-enzyme inhibitors.

The cause is unclear but involves immune stimulation of epidermal keratinocytes; T cells seem to play a central role. Family history is common, and certain genes and HLA antigens (Cw6, B13, B17) are associated with psoriasis. The PSORS1 locus on chromosome 6p21 likely determines a patient's susceptibility of developing psoriasis. An environmental trigger is thought to evoke an inflammatory response and subsequent hyperproliferation of keratinocytes.

Well-identified triggers include:

• Injury (Koebner phenomenon)
• Sunburn
• β-Hemolytic streptococcal infection
• Drugs (especially β-blockers, chloroquine, lithium, ACE inhibitors, indomethacin, terbinafine, and interferon-alfa)
• Emotional stress
• Alcohol consumption
• Tobacco smoking
• Obesity

Psoriasis is an immune-mediated disease associated with a mixed inflammatory dermal infiltrate that initiates and maintains an increase in the proliferation rate of epidermal keratinocytes in affected areas. The increased keratinocyte turnover rate produces epidermal thickening (acanthosis) and disruption of normal epidermal differentiation, resulting in scaling. Disease onset and flares often follow upper respiratory infections (e.g., streptococcal pharyngitis), suggesting that superantigen activation of pathogenic T lymphocytes or molecular mimicry of cutaneous antigens plays a role in pathogenesis.

Symptoms and Signs of Psoriasis

Lesions are either asymptomatic or pruritic and are most often localized on the scalp, extensor surfaces of the elbows and knees, sacrum, buttocks (commonly the gluteal cleft), and genitals. The nails, eyebrows, axillae, umbilicus, and perianal region may also be affected. The disease can be widespread, involving confluent areas of skin extending between these regions. Lesions differ in appearance depending on type.

Among the various psoriasis subtypes, plaque psoriasis (psoriasis vulgaris or chronic plaque psoriasis) accounts for about 90%; lesions are discrete, erythematous papules or plaques covered with thick, silvery, shiny scales. Lesions appear gradually and remit and recur spontaneously or with the appearance and resolution of triggers.

Arthritis develops in 5 to 30% of patients and can be disabling (psoriatic arthritis); joint destruction may ultimately occur.

Psoriasis is rarely life-threatening but can affect a patient’s self-image. Besides the patient's appearance, the sheer amount of time required to treat extensive skin or scalp lesions and to maintain clothing and bedding may adversely affect quality of life.

Clinical features
1. Plaque-type psoriasis occurs as raised erythematous plaques covered with a white scale. Scratching the scale may lead to punctate bleeding (the Auspitz sign).
2. The distribution of psoriatic lesions includes the extensor surfaces of the extremities (knees and elbows), scalp, and trunk (particularly the presacral area).
3. Psoriasis may affect the nails and cause pitting of the nail plates, yellow discoloration, and thickening and separation from the nail bed.
4. Lesions often develop at sites of cutaneous injury or trauma (Köebner phenomenon).
5. Guttate (tear-shaped) psoriasis is a clinical variant that develops rapidly, most often after a streptococcal upper respiratory infection. Multiple, small (􏰀1 cm) psoriatic lesions are distributed on the trunk and extremities.
6. Pustular psoriasis is a typically severe clinical variant that presents with sterile pustules appearing within plaques or diffusely. A pustular psoriasis flare may be associated with hypocalcemia.
7. Erythrodermic psoriasis is a severe clinical variant that presents as a generalized erythema with extensive scaling and exfoliation.
8. Psoriatic arthritis of varying severity affects approximately 10% of psoriatic patients.

Diagnosis of Psoriasis
Diagnosis Psoriasis is usually well recognized on clinical inspection of the skin and usually distinguished from other papulosquamous eruptions. Skin biopsy confirms the clinical impression.

Treatment of Psoriasis
Treatment is tailored to the severity of psoriasis, which is usually estimated by the percentage of the body surface area involved. Topical therapies are used in mild cases, and phototherapy and systemic agents are used for moderate-to-severe cases.

1. Topical agents include topical corticosteroids, topical vitamin D3 analogs (calcipotriene), coal tar preparations and topical retinoids. Phototherapy with psoralen plus UV-A light (PUVA) or UV-B light is very effective in cases with generalized skin involvement.

2. Systemic agents include oral retinoids (acitretin), methotrexate (particularly for arthritis), cyclosporine, and biologic agents. Biologic agents include alefacept (a fusion protein that targets T lymphocyte antigen molecule CD2), etanercept (a fusion protein that targets tumor necrosis factor), infliximab (a monoclonal antibody that targets tumor necrosis factor), and ustekinumab (a monoclonal antibody that targets interleukin-12 [IL-12] and IL-23). Systemic corticosteroids should be avoided because of severe rebound flares on withdrawal.


A 38-year-old female presents with an itchy rash she says has been present for the past several months. She has been using over-the-counter hydrocortisone cream with no improvement. On examination she has an oval 12-cm erythematous plaque on her buttocks. The plaque is covered with silvery scales. Which one of the following would be the best initial treatment for her rash?

A. Betamethasone ointment applied twice daily
B. Clotrimazole 1% cream applied twice daily
C. Diclofenac 3% gel applied twice daily
D. Mupirocin 2% ointment applied twice daily

ANSWER: A. This patient has mild plaque psoriasis. Topical corticosteroids, vitamin D analogs, and tazarotene are effective treatments for mild psoriasis. Antimicrobials, anitfungals and diclofenac are not effective treatments.

An 18-year-old woman comes to the clinic because of a 4-month history of a "red rash" on her elbows, knees, and around her "belly button." She noticed the lesions during the winter, but was not particularly concerned because they were covered up by pants and long sleeves. Now it is summer and she is too embarrassed to wear shorts or a bathing suit. She has no significant past medical history, is up-to-date on her immunizations, and has not traveled recently. She takes no medications and has no known allergies. She tries to avoid all sun exposure because she tends to "burn, not tan." Physical examination shows erythematous plaques on her elbows, knees, and umbilicus. There is a silvery scale covering the majority of each lesion that bleed when you scrape it. The remainder of the examination is unremarkable. The most appropriate next step is to

 A. advise her to avoid sun exposure, especially direct sunlight on the lesions
 B. biopsy each lesion and send for histologic evaluation
 C. inject each lesion with a medium-potency corticosteroid
 D. prescribe a medium-potency corticosteroid ointment and topical calcipotriene
 E. refer her to a dermatologist

The correct answer is D. This patient most likely has psoriasis, which is a relatively common skin condition that affects approximately 2% of the population. Psoriasis is characterized by erythematous, thickened plaques with a silvery scale. Scraping of the scale may lead to pinpoint bleeding, often called the Auspitz sign. The diagnosis is usually made by physical examination. The treatment for localized lesions typically begins with a topical corticosteroid and topical calcipotriene (a vitamin D analog that enhances normal keratinization and inhibits epidermal cell proliferation). A topical corticosteroid can also be used with a coal tar product, which possibly suppresses epidermal DNA synthesis, as a first-line therapy. These can be tapered if the lesions subside. If this in ineffective, corticosteroid and anthralin or tazarotene therapy combined with ultraviolet phototherapy should be considered. If this is still ineffective, the patient should be sent to a dermatologist.

It is inappropriate to advise her to avoid sun exposure, especially direct sunlight on the lesions (choice A) because sunlight is thought to be helpful in treating psoriasis. She should be encouraged to obtain natural sunlight exposure for a few minutes a day. But she needs to be advised that unaffected areas should be covered with a sunscreen.

While psoriasis can be diagnosed by a biopsy, it is inappropriate to biopsy each lesion and send for histologic evaluation (choice B). The diagnosis can usually be made based on clinical presentation, especially when the lesions are classic, as they are in this case.

It is inappropriate to inject each lesion with a medium-potency corticosteroid (choice C) at this time. This is usually reserved for psoriasis that is not controlled by topical therapy.

It is not necessary to refer her to a dermatologist (choice E) at this time. Any physician should be able to recognize and treat localized psoriasis. If the treatments are not effective in controlling her disease, you should refer her to a dermatologist.
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Action And Clinical Pharmacology: Propranolol is a non-selective beta-adrenergic receptor blocking drug.

Beta-blockade may result in bronchial constriction by interfering with endogenously or exogenously induced bronchodilation. 

The mechanism of the antihypertensive effects includes decreased cardiac output (Cardiac Output = Stroke Volume x Heart Rate), inhibition of renin release by the kidneys, and diminution of tonic sympathetic nerve outflow from vasomotor centers in the brain.

Indications And Clinical Uses: 

• Hypertension
• Ventricular tachycardia
• Migraine: The prophylaxis of migraine headache
• Essential Tremor


• Bronchospasm, including bronchial asthma. Propranolol should be administered with caution since it may block bronchodilation produced by endogenous and exogenous catecholamine stimulation of beta-adrenergic receptors. 

• Patients with Diabetes and in those subject to Hypoglycemia: Because of its beta-adrenergic blocking activity, propranolol may block premonitory signs and symptoms (pulse rate and pressure changes) of acute hypoglycemia. This is especially important to keep in mind in patients with labile diabetes.

Adverse Reactions: 

• The most serious adverse effects that may be encountered with propranolol are congestive heart failure and bronchospasm.
• Cardiovascular: severe bradycardia
• CNS: insomnia, fatigue, anorexia, anxiety, mental depression, poor concentration
• Respiratory: bronchospasm
• Sexual: reduction or loss of libido


A 66-year-old woman comes to the office because of difficulty sleeping, a decreased appetite, fatigue, an inability to concentrate, and a general "down" mood for the past 2 weeks. She states that she and her husband are going on a 3-week trip to Europe next month, and she "wants to get to the bottom of this" before they go. She has been coming to you since her first child was born, and over the years you have treated her for gastroenteritis, several yeast infections, and most recently, high blood pressure. She has always been a very compliant patient. You notice in her chart that you prescribed propranolol for her hypertension 1 month ago, after trying to control it with weight reduction, smoking cessation, alcohol elimination, salt and fat reduction, and aerobic exercise. Her blood pressure at 3 previous visits was 150/90 mm Hg and today it is 135/80 mm Hg. She does not take any other medications. At this time you should

A. advise her to start a "gentle" walking routine to "lift her spirits"
B. advise her to stop taking propranolol and give her a prescription for hydrochlorothiazide
C. explain to the patient that she is stressed about her trip, and these symptoms will pass
D. give her a prescription for tranylcypromine
E. increase the dose of propranolol and prescribe phenelzine

The correct answer is B. The symptoms of change in appetite, fatigue, insomnia, lack of concentration, and worthlessness for greater than 2 weeks are consistent with depression. Propranolol is one of the most common pharmacological agents to cause depression. Other side effects of propranolol include dizziness, bronchospasm, nausea, vomiting, diarrhea, and constipation. It may also precipitate asthma, congestive heart failure, and hypoglycemia in susceptible patients. The patient should be switched to another antihypertensive agent.

Just advising her to start a "gentle" walking routine to "lift her spirits" (choice A) is inappropriate because she is having real depressive symptoms that are most likely due to the propranolol.

It is inappropriate to explain to the patient that she is stressed about her trip, and these symptoms will pass (choice C). She is obviously having real symptoms that require serious attention, and in this case the depressive symptoms are most likely due to propranolol.

It is inappropriate to give her a prescription for tranylcypromine (choice D) because her depressive symptoms are most likely due to propranolol. Also, tranylcypromine, which is an MAOI, is not the best first choice for an antidepressive agent due to the necessary dietary restrictions and the risk of orthostatic hypotension. If you were going to give her an antidepressant, an SSRI or a tricyclic, such as nortriptyline, is better because of the relatively low risk of orthostatic hypotension or anticholinergic effects.

Since propranolol is most likely causing her depressive symptoms, it is incorrect to increase the dose of propranolol and prescribe phenelzine (choice E). Also, phenelzine, which is an MAOI, is not the best first choice for an antidepressive agent due to the necessary dietary restrictions and the risk of orthostatic hypotension.

A 32-year-old woman comes to the office "for a prescription of propranolol for stage fright." She tells you that she is professional singer and lately she has been experiencing "butterflies" and palpitations before performances. She has been so worried about having one of these symptoms that she is having trouble sleeping at night. She tells you that a friend of hers has a similar problem and propranolol has "cured her." She has been a patient of yours for the past 10 years and you remember that she has severe asthma, requiring many hospitalizations, the most recent being 2 weeks ago. Her asthma attacks have been increasingly more severe and have been occurring at an increased frequency. She tells you that she is in a rush and all she needs is the prescription. The most appropriate next step is to

A. administer a pulmonary function test
B. explain that propranolol is not a good drug for her
C. give her a referral to a psychiatrist
D. order a chest x-ray
E. prescribe propranolol for her to take before her performances

The correct answer is B. This patient most likely has performance anxiety, which is a form of social phobia. The treatment usually involves beta-blockers before a performance to decrease the symptoms. However, a patient with severe asthma should avoid beta-blockers because they can cause bronchoconstriction and precipitate into an asthmatic attack.

A pulmonary function test (choice A) and a chest x-ray (choice D) are not indicated at this time. You already know that she has asthma that has required hospitalizations and the results of these tests are unlikely to change your management.

A referral to a psychiatrist (choice C) may be helpful in treating her performance anxiety, but she is in your office for propranolol, so it is your responsibility to first try to explain to her that her asthma makes her a bad candidate for this treatment.

You should not prescribe propranolol for her to take before her performances (choice E) because she has severe asthma, which makes beta-blockers a dangerous medication for her. Beta-blockers can cause airway obstruction, which may lead to worsening asthma.

A 43-year-old, insulin-dependent diabetic patient is diagnosed with hypertension and begins therapy with an antihypertensive agent. Three days later, he measures his blood glucose at home and finds that it is 53 mg/dL. He recalibrates his glucose testing apparatus and repeats the test, only to find that the first reading was accurate. He is concerned that his hypoglycemia did not produce the normal premonitory signs and symptoms. Which of the following medications was most likely prescribed to treat his hypertension?

A. Captopril
B. Diltiazem
C. Methyldopa
D. Prazosin
E. Propranolol

The correct answer is E. Beta-adrenergic blockade may blunt or prevent the premonitory signs and symptoms (e.g., tachycardia, blood pressure changes) of acute episodes of hypoglycemia. Non-selective beta-blockers, such as propranolol, may even potentiate insulin-induced hypoglycemia. Even though this effect is less likely with cardioselective agents, the use of either cardioselective or non-selective beta-blockers in diabetics is not recommended due to their "masking" effect of the normal warning signs and symptoms of hypoglycemia. None of the drugs listed in the other choices will blunt the premonitory signs and symptoms of hypoglycemia.

Captopril (choice A) is an angiotensin-converting enzyme (ACE) inhibitor that can be safely used for the treatment of hypertension in diabetic patients. Diltiazem (choice B) is a calcium channel blocker that is also considered to be safe and effective for the treatment of hypertension in diabetic patients. 

Both methyldopa (choice C), a centrally acting alpha-adrenergic agonist, and prazosin (choice D), an alpha1-adrenergic antagonist, can be safely used to treat hypertension in diabetic patients. However, due to the side effect profile of these medications, they are generally used only in diabetic patients who are unresponsive to ACE inhibitors and calcium channel blockers.
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Gonorrhea is caused by the bacteria Neisseria gonorrhoeae. It typically infects epithelia of the urethra, cervix, rectum, pharynx, or eyes, causing irritation or pain and purulent discharge. Dissemination to skin and joints, which is uncommon, causes sores on the skin, fever, and migratory polyarthritis or pauciarticular septic arthritis. Diagnosis is by microscopy, culture, or nucleic acid amplification tests. Several oral or injectable antibiotics can be used, but drug resistance is an increasing problem.

N. gonorrhoeae is a gram-negative diplococcus that occurs only in humans and is almost always transmitted by sexual contact. Urethral and cervical infections are most common, but infection in the pharynx or rectum can occur after oral or anal intercourse, and conjunctivitis may follow contamination of the eye. After an episode of vaginal intercourse, likelihood of transmission from women to men is about 20%, but from men to women, it may be higher. Neonates can acquire conjunctival infection during passage through the birth canal, and children may acquire gonorrhea as a result of sexual abuse.

In 10 to 20% of women, cervical infection ascends via the endometrium to the fallopian tubes (salpingitis) and pelvic peritoneum, causing pelvic inflammatory disease. Chlamydiae or intestinal bacteria may also cause PID. Gonorrheal cervicitis is commonly accompanied by dysuria or inflammation of Skene ducts and Bartholin glands. In a small fraction of men, ascending urethritis progresses to epididymitis. Disseminated gonococcal infection (DGI) due to hematogenous spread occurs in < 1% of cases, predominantly in women. DGI typically affects the skin, tendon sheaths, and joints. Pericarditis, endocarditis, meningitis, and perihepatitis occur rarely.

Coinfection with Chlamydia trachomatis occurs in 15 to 25% of infected heterosexual men and 35 to 50% of women.

Symptoms and Signs

About 10 to 20% of infected women and very few infected men are asymptomatic. About 25% of men have minimal symptoms.

Male urethritis has an incubation period from 2 to 14 days. Onset is usually marked by mild discomfort in the urethra, followed by more severe penile tenderness and pain, dysuria, and a purulent discharge. Urinary frequency and urgency may develop as the infection spreads to the posterior urethra. Examination detects a purulent, yellow-green urethral discharge, and the meatus may be inflamed.

Epididymitis usually causes unilateral scrotal pain, tenderness, and swelling. Rarely, men develop abscesses of Tyson and Littre glands, periurethral abscesses, or infection of Cowper glands, the prostate, or the seminal vesicles.

Cervicitis usually has an incubation period of > 10 days. Symptoms range from mild to severe and include dysuria and vaginal discharge. During pelvic examination, clinicians may note a mucopurulent or purulent cervical discharge, and the cervical os may be red and bleed easily when touched with the speculum. Urethritis may occur concurrently; pus may be expressed from the urethra when the symphysis pubis is pressed or from Skene ducts or Bartholin glands. Rarely, infections in sexually abused prepubertal girls cause dysuria, purulent vaginal discharge, and vulvar irritation, erythema, and edema.

PID occurs in 10 to 20% of infected women. PID may include salpingitis, pelvic peritonitis, and pelvic abscesses and may cause lower abdominal discomfort (typically bilateral), dyspareunia, and marked tenderness on palpation of the abdomen, adnexa, or cervix.

Disseminated gonococcal infection (DGI) , also called the arthritis-dermatitis syndrome, reflects bacteremia and typically manifests with fever, migratory pain or joint swelling (polyarthritis), and pustular skin lesions. In some patients, pain develops and tendons (eg, at the wrist or ankle) redden or swell. Skin lesions occur typically on the arms or legs, have a red base, and are small, slightly painful, and often pustular. Genital gonorrhea, the usual source of disseminated infection, may be asymptomatic. DGI can mimic other disorders that cause fever, skin lesions, and polyarthritis (eg, the prodrome of hepatitis B infection or meningococcemia); some of these other disorders also cause genital symptoms.

Gonococcal septic arthritis is a more localized form of DGI that results in a painful arthritis with effusion, usually of 1 or 2 large joints such as the knees, ankles, wrists, or elbows. Some patients present with or have a history of skin lesions of DGI. Onset is often acute, usually with fever, severe joint pain, and limitation of movement. Infected joints are swollen, and the overlying skin may be warm and red.

• Gram staining and culture
• Nucleic acid–based testing

Gonorrhea is diagnosed when gonococci are detected via microscopic examination using Gram stain, culture, or a nucleic acid–based test of genital fluids, blood, or joint fluids (obtained by needle aspiration).

Gram stain is sensitive and specific for gonorrhea in men with urethral discharge; gram-negative intracellular diplococci typically are seen. Gram stain is much less accurate for infections of the cervix, pharynx, and rectum and is not recommended for diagnosis at these sites.

Culture is sensitive and specific, but because gonococci are fragile and fastidious, samples taken using a swab need to be rapidly plated on an appropriate medium (eg, modified Thayer-Martin) and transported to the laboratory in a CO 2 -containing environment. Blood and joint fluid samples should be sent to the laboratory with notification that gonococcal infection is suspected. Because nucleic acid amplification tests (NAAT) have replaced culture in most laboratories, finding a laboratory that can provide culture and sensitivity testing may be difficult and require consultation with a public health or infectious disease specialist.

Unamplified nucleic acid–based tests may be done on genital, rectal, or oral swabs. Most tests simultaneously detect gonorrhea and chlamydial infection and then differentiate between them in a subsequent specific test. Nucleic acid amplification tests (NAAT) further increase the sensitivity adequately to enable testing of urine samples in both sexes.

In the US, confirmed cases of gonorrhea, chlamydial infection, and syphilis must be reported to the public health system. Serologic tests for syphilis (STS) and HIV and NAAT to screen for chlamydial infection should also be done.

Men with urethritis

Men with obvious discharge may be treated presumptively if likelihood of follow-up is questionable or if clinic-based diagnostic tools are not available. Samples for Gram staining can be obtained by touching a swab or slide to the end of the penis to collect discharge. Gram stain does not identify chlamydiae, so urine or swab samples for NAAT are obtained.

Women with genital symptoms or signs

A cervical swab should be sent for culture or nucleic acid–based testing. If a pelvic examination is not possible, NAAT of a urine sample can detect gonococcal (and chlamydial) infections rapidly and reliably.

Pharyngeal or rectal exposures (either sex)

Swabs of the affected area are sent for culture or nucleic acid–based tests.

Arthritis, DGI, or both

An affected joint should be aspirated, and fluid should be sent for culture and routine analysis. Patients with skin lesions, systemic symptoms, or both should have blood, urethral, cervical, and rectal cultures or NAAT. In about 30 to 40% of patients with DGI, blood cultures are positive during the first week of illness. With gonococcal arthritis, blood cultures are less often positive, but cultures of joint fluids are usually positive. Joint fluid is usually cloudy to purulent because of large numbers of WBCs (typically > 20,000/μL).


• For uncomplicated infection, a single dose of ceftriaxone plus azithromycin or doxycycline
• For DGI with arthritis, a longer course of parenteral antibiotics
• Concomitant treatment for chlamydial infection
• Treatment of sex partners

Uncomplicated gonococcal infection of the urethra, cervix, rectum, and pharynx is treated with a single dose of ceftriaxone 250 mg IM plus azithromycin 1 g po once or doxycycline 100 mg po bid for 7 days. Azithromycin or doxycycline is given to treat coinfection with chlamydiae and possibly to slow development of resistance to ceftriaxone. Monotherapy and previous oral regimens of fluoroquinolones (eg, ciprofloxacin, levofloxacin, ofloxacin) or cefixime are no longer recommended because of increasing drug resistance.

DGI with gonococcal arthritis is initially treated with IM or IV antibiotics (eg, ceftriaxone 1 g IM or IV q 24 h, ceftizoxime 1 g IV q 8 h, cefotaxime 1 g IV q 8 h) continued for 24 to 48 h once symptoms lessen, followed by 4 to 7 days of oral therapy. Antichlamydial therapy is also routinely given.

Gonococcal arthritis does not usually require joint drainage. Initially, the joint is immobilized in a functional position. Passive range-of-motion exercises should be started as soon as patients can tolerate them. Once pain subsides, more active exercises, with stretching and muscle strengthening, should begin. Over 95% of patients treated for gonococcal arthritis recover complete joint function. Because sterile joint fluid accumulations (effusions) may persist for prolonged periods, an anti-inflammatory drug may be beneficial.

Sex partners

All sex partners who have had sexual contact with the patient within 60 days should be tested for gonorrhea and other STDs and treated if results are positive. Sex partners with contact within 2 wk should be treated presumptively for gonorrhea (epidemiologic treatment).

Key Points
• Gonorrhea typically causes uncomplicated infection of the urethra, cervix, rectum, pharynx, and/or eyes.
• Sometimes gonorrhea spreads to the adnexa, causing salpingitis, or disseminates to skin and/or joints, causing skin sores or septic arthritis.
• Diagnose using NAAT, but culture and sensitivity testing should be done when needed to detect antimicrobial resistance.
• Screen asymptomatic, high-risk patients using NAAT.
• Treat uncomplicated infection with a single dose of ceftriaxone 250 mg IM plus either azithromycin 1 g po once or doxycycline 100 mg po bid for 7 days.


An 18-year-old girl comes to the clinic because of a 3-day history of vaginal discharge. The discharge is malodorous & has a greenish-yellow color. She admits to sexual intercourse with a "random guy at a fraternity party" 5 days earlier. Physical examination shows a malodorous, purulent vaginal discharge. Complete physical & pelvic examinations are unremarkable. A Gram stain of the discharge shows Gram-negative diplococci within polymorphonuclear leukocytes. Culture on a chocolate agar confirms the diagnosis. The most appropriate next step is to

A. admit her to the hospital for intravenous therapy with cefotetan
B. contact the board of health to report a case of gonorrhea
C. contact the "random guy at a fraternity party" and provide treatment and counseling
D. give her a single dose of ceftriaxone, intramuscularly and a single dose of azithromycin, orally
E. prescribe metronidazole for this patient and her sexual partner

The correct answer is D. This patient has a gonococcal infection and should be treated with a single dose of ceftriaxone, intramuscularly and a single dose of azithromycin, orally. The ceftriaxone treats the gonococcal infection and the azithromycin is added for the presumptive treatment of Chlamydia trachomatis. This is because many patients have co-existing infections. After treating the patient, this case should be reported to the board of health because gonorrhea is a notifiable infectious disease. Sexual contacts should be treated and counseled.

It is unnecessary to admit her to the hospital for intravenous therapy with cefotetan (choice A). This is part of the treatment of pelvic inflammatory disease, which is a disease of the upper genital tract. Patients often have cervical motion tenderness, lower abdominal tenderness, and adnexal tenderness, fever, cervical discharge, and laboratory documentation of N. Gonorrhea and/or C. trachomatis. These patients are treated with a cephalosporin for gonorrhea and doxycycline for chlamydia. This patient seems to have an uncomplicated gonococcal infection that can be treated as an outpatient.

Since gonorrhea is a notifiable disease, it is necessary to contact the board of health to report a case of gonorrhea (choice B) after treating the patient with the appropriate antibiotics.

The "random guy at a fraternity party" should be contacted to provide treatment and counseling (choice C) after treating the patient with the appropriate antibiotics.

It is incorrect to prescribe metronidazole for this patient and her sexual partner (choice E) because this is the treatment for Trichomonas vaginalis, not gonorrhea. Trichomonas vaginalis often presents with a frothy vaginal discharge. A wet mount shows motile flagellated organisms. Gram-negative diplococci within polymorphonuclear leukocytes are not found in this infection.

A 25-year-old man presents with complaints of dysuria for the past 6 days. He has had multiple female sexual partners in the past 2 months. Physical examination shows a yellowish penile discharge with inguinal adenopathy but no genital ulcers. Gram’s stain of the discharge shows intracellular gram-negative diplococci in leukocytes. Which one of the follow- ing should be used in the treatment of this patient?

A. Ceftriaxone
B. Ciprofloxacin
C. Procaine penicillin
D. Ceftriaxone plus doxycycline 
E. Doxycycline

The answer is D. This patient has gonococcal urethritis (GCU), which is caused by Neisseria gonorrhoeae. GCU is more common among homosexual men and those of the lower socioeconomic strata. Nongonococcal urethritis (NGU) on the other hand, is more commonly encountered in heterosexual males and those of higher socioeconomic class. NGU is twice as common as gonococcal urethritis in the United States; it is the most common sexually transmitted disease (STD) in men and is usually due to Chlamydia trachomatis. However, Trichomonas vaginalis or herpes simplex virus (HSV) can also cause NGU. At one time, the standard treatment would have been penicillin (choice C). However, because of increasing resistance, penicillin is no longer recommended for gonorrhea. Ceftriaxone (choice A) and cefixime are drugs that inhibit cell wall synthesis and are not susceptible to 􏰅-lactase hydrolysis; therefore, they are recommended replacements for penicillin in the treatment of gonorrhea. The quinolones, ciprofloxacin (choice B) and ofloxacin, inhibit bacterial DNA gyrase and have a relatively broad spectrum of activity. They too are effective against gonorrhea. However, because chlamydi- al infections so often accompany gonococcal infections, the Centers for Disease Control (CDC) recommends

that all patients with suspected or proved gonococcal urethritis also be treated as if they had chlamydial NGU. Although the quinolones have antichlamydial activity in vitro, they have not been recommended for clinical infections. C. trachomatis is susceptible to tetracyclines such as doxycycline (choice E), but strains of tetracy- cline-resistant N. gonorrhoeae have also become too common to recommend its use. Therefore, combined therapy, such as ceftriaxone and doxycycline (choice D), is required to treat both infections. Alternatively, because both organisms are still susceptible to the relatively new drug azithromycin, it can be used alone.
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Hyperkalemia is serum K concentration > 5.5 mEq/L resulting from excess total body K stores or abnormal movement of K out of cells. There are usually several simultaneous contributing factors, including increased K intake, drugs that impair renal K excretion, and acute or chronic kidney disease. It can also occur in metabolic acidosis as in diabetic ketoacidosis. Clinical manifestations are generally neuromuscular, resulting in muscle weakness and cardiac toxicity that, when severe, can degenerate to ventricular fibrillation or asystole. Diagnosis is by measuring serum K. Treatment may involve decreasing K intake, adjusting drugs, giving a cation exchange resin and, in emergencies, Ca gluconate, insulin and dialysis.

The most common cause of increased serum K concentration is probably pseudohyperkalemia caused by hemolysis of RBCs in the blood sample. Normal kidneys eventually excrete K loads, so sustained, nonartifactual hyperkalemia usually implies diminished renal K excretion. However, other factors usually contribute. They can include increased K intake, increased K release from cells, or both. When sufficient KCl is ingested or given parenterally, severe hyperkalemia may result even when renal function is normal but is usually temporary.

Hyperkalemia due to total body K excess is particularly common in oliguric states (especially acute kidney injury) and with rhabdomyolysis, burns, bleeding into soft tissue or the GI tract, and adrenal insufficiency. In chronic kidney disease, hyperkalemia is uncommon until the GFR falls to < 10 to 15 mL/min unless dietary or IV K intake is excessive.

Symptoms and Signs
Many individuals with hyperkalemia are asymptomatic. When present, symptoms are nonspecific and predominantly related to muscular or cardiac function. Weakness and fatigue are the most common complaints. Occasionally, patients may report the following: Frank muscle paralysis, Dyspnea, Palpitations, Chest pain, Nausea or vomiting and Paresthesias.

In general, the results of the physical examination alone do not alert the physician to the diagnosis of hyperkalemia, except when severe bradycardia is present or muscle tenderness accompanies muscle weakness, suggesting rhabdomyolysis. Examination findings in patients with hyperkalemia include the following:

• Vital signs usually normal, except occasionally in bradycardia due to heart block or tachypnea due to respiratory muscle weakness
• Muscle weakness and flaccid paralysis
• Depressed or absent deep tendon reflexes

When hyperkalemia is discovered, investigate potential pathophysiologic mechanisms. Hyperkalemia can result from any of the following, which often occur in combination:

• Excessive intake
• Decreased excretion
• A shift of potassium from the intracellular to the extracellular space

• Serum K measurement
• Review of drug use
• Assessment of renal function

Hyperkalemia (serum K > 5.5 mEq/L) may be found on routine serum electrolyte measurement. It should be suspected in patients with typical changes on an ECG or patients at high risk, such as those with renal failure, advanced heart failure, or urinary obstruction, or treated with ACE inhibitors and K-sparing diuretics.

ECG should be done on patients with hyperkalemia. ECG changes are frequently visible when serum K is > 5.5 mEq/L. Slowing of conduction characterized by an increased PR interval and shortening of the QT interval as well as tall, symmetric, peaked T waves are visible initially. K > 6.5 mEq/L causes further slowing of conduction with widening of the QRS interval, disappearance of the P wave, and nodal and escape ventricular arrhythmias. Finally, the QRS complex degenerates into a sine wave pattern, and ventricular fibrillation or asystole ensues.

Diagnosis of cause

Pseudohyperkalemia should be considered in patients without risk factors or ECG abnormalities. Hemolysis may be reported by the laboratory. When pseudohyperkalemia is suspected, K concentration should be repeated, taking measures to avoid hemolysis of the sample.

Diagnosis of the cause of hyperkalemia requires a detailed history, including a review of drugs, a physical examination with emphasis on volume status, and measurement of electrolytes, BUN, and creatinine. In cases in which renal failure is present, additional tests, including renal ultrasonography to exclude obstruction, are needed.


• Treatment of the cause
• For mild hyperkalemia, Na polystyrene sulfonate
• For moderate or severe hyperkalemia, IV insulin and glucose, an IV Ca solution, possibly an inhaled β 2 -agonist, and usually hemodialysis

Mild hyperkalemia

Patients with serum K < 6 mEq/L and no ECG abnormalities may respond to diminished K intake or stopping K-elevating drugs. The addition of a loop diuretic enhances renal K excretion as long as volume depletion is not present.

Na polystyrene sulfonate in sorbitol can be given (15 to 30 g in 30 to 70 mL of 70% sorbitol po q 4 to 6 h). It acts as a cation exchange resin and removes K through the GI mucosa. Sorbitol is administered with the resin to ensure passage through the GI tract. Patients unable to take drugs orally because of nausea or other reasons may be given similar doses by enema. Enemas are not as effective at lowering K in patients with ileus. Enemas should not be used if acute abdomen is suspected. About 1 mEq of K is removed per gram of resin given. Resin therapy is slow and often fails to lower serum K significantly in hypercatabolic states. Because Na is exchanged for K when Na polystyrene sulfonate is used, Na overload may occur, particularly in oliguric patients with preexisting volume overload.

Moderate to severe hyperkalemia

Serum K between 6 and 6.5 mEq/L needs prompt attention, but the actual treatment depends on the clinical situation. If no ECG changes are present and renal function is intact, maneuvers as for mild hyperkalemia are usually effective. Follow-up serum K measurements are needed to ensure that the hyperkalemia has been successfully treated. If serum K is > 6.5 mEq/L, more aggressive therapy is required. Administration of regular insulin 5 to 10 units IV is followed immediately by or administered simultaneously with rapid infusion of 50 mL 50% glucose. Infusion of 10% D/W should follow at 50 mL/h to prevent hypoglycemia. The effect on serum K peaks in 1 h and lasts for several hours.

If ECG changes include the loss of P-wave or widening of the QRS complex, treatment with IV Ca as well as insulin and glucose is indicated; 10 to 20 mL 10% Ca gluconate (or 5 to 10 mL 22% Ca gluceptate) is given IV over 5 to 10 min. Ca antagonizes the effect of hyperkalemia on cardiac muscle. Ca should be given with caution to patients taking digoxin because of the risk of precipitating hypokalemia-related arrhythmias. If the ECG shows a sine wave pattern or asystole, Ca gluconate may be given more rapidly (5 to 10 mL IV over 2 min). CaCl can also be used but can be irritating to peripheral veins and cause tissue necrosis if extravasated. CaCl should be given only through a correctly positioned central venous catheter. The benefits of Ca occur within minutes but last only 20 to 30 min. Ca infusion is a temporizing measure while awaiting the effects of other treatments or initiation of hemodialysis and may need to be repeated.

A high-dose β 2 -agonist, such as albuterol 10 to 20 mg inhaled over 10 min (5 mg/mL concentration), can lower serum K by 0.5 to 1.5 mEq/L and may be a helpful adjunct. The peak effect occurs in 90 min. However, β 2 -agonists are contraindicated in patients with unstable angina or acute MI.

Administration of IV NaHCO 3 is controversial. It may lower serum K over several hours. Reduction may result from alkalinization or the hypertonicity due to the concentrated Na in the preparation. The hypertonic Na that it contains may be harmful for dialysis patients who also may have volume overload. When given, the usual dose is 45 mEq (1 ampule of 7.5% NaHCO 3 ) infused over 5 min and repeated in 30 min. HCO 3 therapy has little effect when used by itself in patients with severe renal insufficiency unless acidemia is also present.

In addition to strategies for lowering K by shifting it into cells, maneuvers to remove K from the body should also be done early in the treatment of severe or symptomatic hyperkalemia. K can be removed via the GI tract by administration of Na polystyrene sulfonate or by hemodialysis. Hemodialysis should be instituted promptly after emergency measures in patients with renal failure or when emergency treatment is ineffective. Dialysis should be considered early in patients with end-stage renal disease and hyperkalemia because they are at increased risk of progression to more severe hyperkalemia and serious cardiac arrhythmias. Peritoneal dialysis is relatively inefficient at removing K.

Key Points
• Common causes of hyperkalemia include K-retaining drugs, renal insufficiency, adrenal insufficiency, and disorders involving cellular breakdown (eg, rhabdomyolysis, burns, bleeding into soft tissue or the GI tract).
• Hyperkalemia is usually asymptomatic until cardiac toxicity develops, although some patients have weakness.
• ECG changes begin with an increased PR interval, shortening of the QT interval, and tall, symmetric, peaked T waves; with K > 6.5 mEq/L, QRS interval widens, and P wave disappears; ultimately, the QRS complex degenerates into a sine wave pattern, and ventricular fibrillation or asystole ensues.
• Give Na polystyrene sulfonate for mild hyperkalemia.
• Give IV insulin, glucose, and Ca, and possibly an inhaled β 2 -agonist for moderate to severe hyperkalemia.
• Use hemodialysis for patients with chronic kidney disease and those with significant ECG changes.


A 60-year-old man with diabetes mellitus, hypertension, hyperlipidemia, and chronic renal insufficiency is admitted to the hospital because of lightheadedness. His medications include NPH insulin, amlodipine, and simvastatin. He is allergic to penicillin to which he gets an angioedema. His temperature is 37.1 C (98.8 F), blood pressure is 98/65 mm Hg, pulse is 87/min, and his respiratory rate is 22/min. On exam, he is ill appearing. His cardiac rhythm is regular and breath sounds are clear bilaterally. His abdominal exam is benign. A chest radiograph shows clear lungs. An electrocardiogram shows a sinus rhythm with peaked T waves. Laboratory studies show a serum sodium of 134 mEq/L, glucose of 98 mg/dL, and potassium of 6.2 mEq/L. The most appropriate intervention at this time is

A. administration of glucose, orally
B. administration of insulin and glucose, intravenously
C. administration of furosemide, orally
D. administration of ringers lactate, intravenously
E. administration of sodium chloride, intravenously

The correct answer is B. Hyperkalemia with electrocardiographic changes (peaked T waves) requires immediate medical treatment to prevent the onset of hyperkalemia-induced dysrhythmias. Administration of insulin intravenously causes serum potassium to move intracellularly, acutely reducing serum potassium. Glucose is co-administered to prevent insulin-induced hypoglycemia.

Oral glucose (choice A) is of no utility in the treatment of hyperglycemia. Even when insulin is used for the treatment of hyperkalemia, glucose should be co-administered intravenously. Oral furosemide (choice C) is an appropriate choice for the long-term treatment of hyperkalemia, i.e., once the acute hyperkalemia has been treated. Interventions such as insulin and glucose simply cause the potassium to shift intracellularly. Its excretion can then be promoted by administration of diuretic agents such as furosemide.

Ringers lactate (choice D) should be avoided with hyperkalemic patients since it contains potassium as a constituent (4 mEq/L). Sodium chloride (choice E) is not useful in the management of hyperkalemia.

A 48-year-old patient presents to the emergency room with a history of tiredness, vomiting, and abdominal pain. He has a long history of hypertension, diabetes mellitus, and hyperlipidemia, and during this past year, he developed end-stage renal disease. He admits to being depressed of late and has not kept his appointment with the nephrologist for renal dialysis, which he used to go to three times a week. The patient is on medications for hypertension, diabetes, and hyperlipidemia, in addition to medications for renal failure. Which of the following is the initial medication that should be administered to reverse the clinical condition reflected by the accompanying electrocardiogram pattern?

A. Sodium bicarbonate 
B. Furosemide
C. Calcium gluconate 
D. Glucose plus insulin 
E. Cation-exchange resin

The answer is C. The electrocardiogram (ECG) pattern shown indicates that this patient has hyperkalemia. It reveals tall, slender, tented T waves in leads I, II, aVF, and V2 through V6. Other findings suggesting hyperkalemia include a widened QRS complex and even biphasic QRS-T complexes. Although hyperkalemia produces these characteristic patterns, the ECG is not a sensitive indicator of hyperkalemia, as almost 50% of patients with serum potassium levels above 6.5 mEq/L do not show any changes in the ECG pattern. This is because atrial cells are more sensitive than ventricular cells to elevated levels of potassium, permitting normal conduction even if atrial depolarization is inhibited; as a result, a junctional rhythm can result. To avoid dangerous arrhythmias and asystole, hyperkalemia above 6.5 mEq/L warrants immediate correction. In this case, hyperkalemia also is suspected clinically because the patient has end-stage renal disease, has not been undergoing dialysis, and has a history of tiredness, vomiting, and abdominal pain. Hyperkalemia could, in addition, have caused motor paralysis. Calcium gluconate 10% (choice C) or 5% calcium chloride is the initial drug of choice. Approximately 5–30 mL of either administered intravenously provides calcium ion, which acts within minutes to antagonize cardiac conduction abnormalities; the effect lasts approximately an hour. In patients who are on digoxin, one must ensure that they do not have digoxin toxicity; if that were the case, calcium would only increase its toxic effects on the myocardium.

Although administering calcium has a rapid effect, it does not promote the shift of potassium into the cells; consequently, its effect is transitory. To secure a more permanent effect, one usually follows up with insulin and glucose (choice D). This drives potassium into the cells, thereby lowering serum potassium levels. Regular insulin (5–10 units) combined with 25 g of 50% glucose is administered intravenously. Insulin takes about 15 minutes to an hour to act, and the action lasts anywhere from 4 to 6 hours. Use of sodium bicarbonate (choice A) is an alternative to insulin plus glucose. It creates a metabolic alkalosis, causing potassium ion to enter the cells in exchange for hydrogen ions. One or two ampules of sodium bicarbonate (approximately 44 mEq each) can be administered intravenously. Its effects begin in approximately 15–30 minutes and last anywhere from 1 to 2 hours. Thus, it is not as long lasting as insulin. The use of furosemide (choice B) is inappropriate in an emergency situation because it takes anywhere from 30 minutes to 2 hours to lower potassium levels, and one may very well not have the luxury of time. It is a loop diuretic that exchanges sodium for potassium, expelling the latter in the urine. Like loop diuretics, sodium polystyrene sulfonate in 20% sorbitol, a cation- exchange resin (choice E), may be used in nonemergency situations; 15–30 mL is administered orally or rectally. Potassium ions bind to the resin, lowering serum potassium levels. Due to the mode of administration, it takes much longer to act; its action lasts approximately 3 hours.
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Mucormycosis is an infection of immunosuppressed patients, including those with diabetes. In rhinocerebral mucormycosis, Rhizopus , Rhizomucor , or another angioinvasive fungal species enters the vascular space and causes tissue necrosis of the nasal septum, palate, orbit, and sinuses. The infection can extend into the brain, causing cavernous sinus thrombosis, seizures, and thrombotic stroke.

Mucormycosis refers to infection caused by diverse fungal species, including Rhizopus, Rhizomucor, and Mucor. Symptoms most frequently result from invasive necrotic lesions in the nose and palate, causing pain, fever, orbital cellulitis, proptosis, and purulent nasal discharge. CNS symptoms may follow. Pulmonary symptoms are severe and include productive cough, high fever, and dyspnea. Disseminated infection may occur in severely immunocompromised patients. Diagnosis is primarily clinical, requires a high index of suspicion, and is confirmed by histopathology and culture. Treatment is with IV amphotericin B and surgery to remove necrotic tissue. Even with aggressive treatment, mortality rates are high.

Infection is most common among immunocompromised people, in patients with poorly controlled diabetes (particularly those with ketoacidosis), and in patients receiving the iron-chelating drug deferoxamine.

The most common form of mucormycosis is Rhinocerebral

However, primary cutaneous, pulmonary, or GI lesions sometimes develop, and hematogenous dissemination to other sites can occur. Cutaneous Rhizopus infections have developed under occlusive dressings but more often result from trauma when the injured areas are contaminated with soil.

Symptoms and Signs

Rhinocerebral infections are usually severe and frequently fatal unless diagnosed early and treated aggressively.

Necrotic lesions appear on the nasal mucosa or sometimes the palate. Vascular invasion by hyphae leads to progressive tissue necrosis that may involve the nasal septum, palate, and bones surrounding the orbit or sinuses. Manifestations may include pain, fever, orbital cellulitis, proptosis, purulent nasal discharge, and mucosal necrosis.

Progressive extension of necrosis to the brain can cause signs of cavernous sinus thrombosis, seizures, aphasia, or hemiplegia.

Pulmonary infections resemble invasive aspergillosis. Pulmonary symptoms (eg, productive cough, high fever, dyspnea) are severe.


• Examination of tissue samples for broad, ribbon-like, nonseptate hyphae

• Sputum Culture (if pulmonary involvement)

Diagnosis requires a high index of suspicion and painstaking examination of tissue samples for large nonseptate hyphae with irregular diameters and right-angle branching patterns; the examination must be thorough because much of the necrotic debris contains no organisms. For unclear reasons, cultures may be negative, even when hyphae are clearly visible in tissues.

CT and x-rays often underestimate or miss significant bone destruction.


• Control of underlying condition

• Lipid amphotericin B formulations

• Surgical debridement

Effective therapy requires that diabetes be controlled or, if at all possible, immunosuppression be reversed or deferoxamine be stopped.

A high-dose lipid amphotericin B formulation (7.5 to 10 mg/kg IV once/day) is recommended as initial therapy, although recent evidence suggests that posaconazole may be effective, especially as consolidation therapy. Posaconazole has not been studied as primary therapy.

Complete surgical debridement of necrotic tissue is critical.


A patient is seen by a specialist because of chronic, intractable, sinusitis. The decision is made to treat the patient surgically, with evacuation of sinus contents and dilation of the sinus ostia. The material removed is sent routinely for pathologic examination. An unexpected finding is the presence of fungi with broad, nonseptate, irregularly shaped hyphae. Subsequent review of the patient's chart reveals a long history of poorly controlled diabetes mellitus. Which of the following is the most likely causative organism? 

A. Aspergillus 
B. Blastomyces 
C. Candida 
D. Rhizopus 
E. Sporothrix 

The correct answer is D. The patient has rhinocerebral mucormycosis, which can be caused by fungal species including Rhizopus, Rhizomucor, Absidia, and Basidiobolus. Predisposing conditions include immunosuppression, uncontrolled diabetes mellitus, and patients using the iron-chelating drug desferrioxamine. While these infections occasionally appear more or less incidentally, as in this case, they are very important to diagnose because they have a tendency to become fulminant. The lesions tend to be very locally destructive and can erode into the eye, palate, and central nervous system, often from an initial site in the sinuses. Fulminant infections are frequently fatal. Pulmonary infections can also occur. The organism can be difficult to culture. The appropriate antibiotic is IV amphotericin B, but surgical debridement should also be strongly considered, since penetration of antibiotic into necrotic tissues may be poor. 

Aspergillus(choice A) can also cause sinusitis, but has narrow hyphae. Blastomyces(choice B) usually involves the lung and occurs as a yeast form in the body. 

Candida(choice C) can infect sinuses, but has narrow hyphae and yeast forms. 

Sporothrix(choice E) usually infects the skin and subcutaneous tissues and occurs as a yeast. 

A 68-year-old diabetic man comes to the office because of double vision and a fever. He says that this all started about 3 weeks ago with dull pain over his cheeks, a low-grade fever, and thin, bloody nasal discharge. He says that he has not been feeling "great" since his wife passed away 4 months ago and he has not been very good at checking his "sugars" because that used to be his wife's job. He seems very sad and a bit confused. His temperature is 39.0 C (102.2 F), blood pressure is 120/80 mm Hg, pulse is 70/min, and respirations are 20/min. Physical examination shows proptosis and a reduction of movement of his left eye, an inflamed left cheek, and dusky red nasal turbinates on the left side. His blood glucose level is 269 mg/dL. The most correct statement about his condition is:

A. A biopsy of his nasal turbinates will show invasive squamous cell carcinoma
B. Insulin, intravenous fluids, and potassium replacement will improve his symptoms
C. Infectious invasion of the ophthalmic artery and globe is responsible for his visual signs and symptoms
D. The symptoms on the left side of his face are unrelated to his diabetes mellitus
E. Tight control of his diabetes will reverse the symptoms on the left side of his face

The correct answer is C. This diabetic patient most likely has mucormycosis, which is a fungal infection that typically only affects individuals with a preexisting disease (diabetes). The clinical features are a fever, sinus pain, thin, bloody nasal discharge, double vision with a reduction of movement of his left eye, and red or necrotic nasal turbinates. The fungal invasion of the ophthalmic artery and globe may cause blindness and a direct invasion of the brain may lead to obtundation and coma. A CT scan, MRI, and biopsies are all helpful in establishing the diagnosis and in evaluating the extent of the disease. The treatment involves extensive surgical debridement and amphotericin B. Regulation of the blood glucose levels is an important part of treating the disease.

Since this patient most likely has mucormycosis, it is unlikely that a biopsy of his nasal turbinates will show invasive squamous cell carcinoma (choice A). Nasopharyngeal carcinoma is very rare, but when it does occur, it typically presents with eustachian tube and nasal obstruction. A middle ear effusion may be present. In this patient with poorly controlled diabetes, a high temperature, and the relatively sudden onset of these symptoms, mucormycosis is more likely than nasopharyngeal carcinoma.

Insulin, intravenous fluids, and potassium replacement will improve his symptoms (choice B) is incorrect because this is the treatment for diabetic ketoacidosis, not mucormycosis. This patient needs surgical debridement and amphotericin B.

The symptoms on the left side of his face are unrelated to his diabetes mellitus (choice D) is incorrect because his poorly controlled diabetes is the main risk factor for developing mucormycosis of the paranasal sinuses and nose.

While tight control of his diabetes is important in treating mucormycosis along with debridement and amphotericin B, it alone will not reverse the symptoms on the left side of his face (choice E).

A 29-year old woman comes to the emergency department with her mother because she "cannot see" out of her right eye. A few weeks ago she began to have double vision and nasal congestion, which she attributed to her drug abuse, but the symptoms have been getting progressively worse. Her mother tells you that her daughter is a "poorly controlled diabetic with a heroin problem" and that she has been in and out of rehabilitation centers for years. She does not monitor her glucose levels and admits to "forgetting" to use her insulin when she is "high" which is most of the time. Her temperature is 39.3 C (102.7 F), blood pressure is 110/70 mm Hg, pulse is 75/min, and respirations are 17/min. Physical examination shows proptosis of the right eye, a thin, bloody nasal discharge, and a area of necrosis of the right side of the hard palate that does not cross the midline. A CT scan of the head shows opacification of the frontal sinus. Carotid arteriography shows obstruction of the carotid siphon. The most appropriate next step is to

A. obtain blood cultures
B. obtain a sputum culture and smear
C. perform a lumbar puncture
D. perform a wet mount smear of crushed tissue obtained by a biopsy
E. schedule the patient for immediate surgery

The correct answer is D. This diabetic patient most likely has mucormycosis, which is a fungal infection that typically only affects individuals with a preexisting disease (diabetes). The clinical features are a fever, sinus pain, thin, bloody nasal discharge, double vision with a reduction of movement of her right eye, and red or necrotic nasal turbinates. The fungal invasion of the ophthalmic artery and globe may cause blindness and a direct invasion of the brain may lead to obtundation and coma. A CT scan, MRI, and biopsies are all helpful in establishing the diagnosis and evaluating the extent of the disease. A wet mount made from crushed tissue obtained by biopsy can establish the diagnosis rapidly by showing broad, septated hyphae. The treatment involves extensive surgical debridement and amphotericin B. Regulation of the blood glucose levels is an important part of treating the disease.

Blood cultures (choice A) are negative in cases of craniofacial mucormycosis. A biopsy of the lesion with histological sections and a wet mount of crushed tissue, is necessary to establish the diagnosis.

A sputum culture and smear (choice B) may be helpful in establishing the diagnosis of pulmonary mucormycosis, but not craniofacial mucormycosis.

A lumbar puncture (choice C) with cerebrospinal fluid analysis is not usually helpful in establishing the diagnosis of craniofacial mucormycosis.

Immediate surgery (choice E) for debridement is probably necessary after the diagnosis of craniofacial mucormycosis is established with a biopsy of the lesion.
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Tuberous Sclerosis
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Tuberous sclerosis (TS) is a dominantly inherited genetic disorder in which tumors (usually hamartomas) develop in multiple organs.

TS occurs in 1 of 6000 children; 85% of cases involve mutations in the TSC1 gene (9q34) or the TSC2 gene (16p13.3). If either parent has the disorder, children have a 50% risk of having it. However, new mutations account for two thirds of new cases.

Patients with TS (sometimes called TS complex) have tumors or abnormalities that manifest at different ages and in multiple organs, including the brain, heart, eyes, kidneys, lungs, and skin.

CNS tubers interrupt neural circuits, causing developmental delay and cognitive impairment and may cause seizures, including infantile spasms. Sometimes the tubers grow and obstruct CSF flow from the lateral ventricles, causing unilateral hydrocephalus.. Sometimes tubers undergo malignant degeneration into gliomas, particularly subependymal giant cell astrocytomas.

Cardiac myomas may develop prenatally, sometimes causing heart failure in neonates. These myomas tend to disappear over time and usually do not cause symptoms later in childhood or in adulthood.

Kidney tumors (angiolipomas) may develop in adults, and polycystic kidney disease may develop at any age. Kidney disease may cause hypertension.

Pulmonary lesions, such as lymphangioleiomyomatosis, may develop, particularly in adolescent girls.

Symptoms and Signs
Manifestations vary greatly in severity. Skin lesions are typically present. Fetal ultrasonography may detect cardiac myomas, or infants may present with a type of seizure called infantile spasms. Affected children may also have other types of seizures, intellectual disability, autism, learning disorders, or behavioral problems. Retinal patches are common and may be visible with funduscopy. Pitting of enamel in permanent teeth is common.

Skin findings include:

• Initially pale, ash leaf–shaped macules, which develop during infancy or early childhood
• Angiofibromas of the face (adenoma sebaceum), which develop during later childhood
• Congenital shagreen patches (raised lesions resembling an orange peel), usually on the back
• Subcutaneous nodules
• Café-au-lait spots
• Subungual fibromas, which can develop any time during childhood or early adulthood

• Identification of the skin lesions
• Imaging of affected organs
• Genetic testing

TS may be suspected when fetal ultrasonography detects cardiac myomas or when infantile spasms occur. Physical examination is done to check for typical skin lesions. Cardiac or cranial manifestations may be visible on routine prenatal ultrasonography. MRI or ultrasonography of the affected organs is necessary for confirmation. Specific genetic testing is available.


Prognosis depends on symptom severity. Infants with mild symptoms generally do well and live long, productive lives; infants with severe symptoms may have serious disabilities. Regardless of severity, most children show continued developmental progress.

• Symptomatic treatment
• Everolimus

Treatment is both symptomatic and specific:

• For seizures: Anticonvulsants (especially vigabatrin for infantile spasms) or sometimes epilepsy surgery
• For skin lesions: Dermabrasion or laser techniques
• For neurobehavioral problems: Behavior management techniques or drugs
• For hypertension caused by renal problems: Antihypertensives or surgery to remove growing tumors
• For developmental delays: Special schooling or occupational therapy
• For malignant tumors and some of the benign tumors: Everolimus

All patients should be screened regularly to detect complications early. Typically, the following is done:

• MRI of the head to check for intracranial complications at least every 3 yr
• Renal ultrasonography to check for kidney tumors every 3 yr in school-aged children and every 1 to 2 yr in adults
• Chest x-ray in girls in their late teens
• Neuropsychologic testing periodically in children to help plan for support at school

Use of everolimus to prevent some complications of TS is under study.

Clinical monitoring is also important and sometimes prompts more frequent testing. Development of headaches, loss of skills, or new kinds of seizures may be caused by malignant degeneration or growth of CNS tubers and are indications for neuroimaging.

Genetic counseling is indicated for adolescents and adults of childbearing age.


A 10-year-old boy with history of epilepsy and mental retardation is brought to a specialty clinic for evaluation. Physical examination is remarkable for several ovoid hypopigmented areas on the trunk and large numbers of red and yellow papules on the face, particularly near the mouth. Biopsy of the papules demonstrates angiofibromata. This patient is most likely to have which of the following central nervous system pathologies?

A. Acoustic neuromas
B. Capillary hemangioblastomas
C. Herniation of cerebellar tonsils into foramen magnum
D. Large cortical hamartomas
E. Leptomeningeal angiomatosis

The correct answer is D. The disease is tuberous sclerosis. The facial angiofibromata are also called adenoma sebaceum, and the hypopigmented patches on the trunk are called ash-leaf spots. This disease is one of the neurocutaneous disorders called phacomatoses. Tuberous sclerosis is inherited as an autosomal dominant trait, and epilepsy and mental retardation are commonly seen in this disorder. Large, firm, white hamartomatous nodules (tubers) are seen in the cortex and in subependymal sites. The tubers consist of aberrantly arranged neurons and/or glia. Patients may also have pancreatic cysts, renal angiomyolipomas, and cardiac rhabdomyomas. Rarely, an astrocytoma will arise in a tuber.

Acoustic neuromas (choice A) are a feature of neurofibromatosis Type II.

 Capillary hemangioblastomas (choice B) are a feature of Von Hippel-Lindau syndrome.

Herniation of cerebellar tonsils (choice C) is a feature of Arnold-Chiari malformation. 

Leptomeningeal angiomatosis (choice E) is a feature of Sturge-Weber disease.

A young mother brings in her 3-year-old daughter to the clinic because of worsening acne problems on her daughter's face. She had a normal birth without complications. However, she is developmentally slow and has had a few episodes of seizures of unknown etiology. Her medications include phenytoin and a multivitamin. The child is playful and her size and weight are appropriate for her age. She has numerous firm, flesh-colored papules scatter over her nose, both cheeks, and chin. There are no pustules or inflammatory papules. She also has multiple, small, hypopigmented ash leaf and confetti-type macules on both lower extremities. The rest of her examination is unremarkable. The next most appropriate step is to

A. check morning level of cortisol
B. check serum level of DHEAS and testosterone
C. prescribe oral minocycline
D. prescribe topical benzoyl peroxide every morning and topical erythromycin every evening
E. send her for an x-ray of the skull

The correct answer is E. An x-ray of the skull is the most appropriate next step, because this patient has tuberous sclerosis (TS). TS is also known as epiloia (epi = epilepsy, loi = low intelligence, a = adenoma sebaceum). This is an autosomal dominant syndrome marked by other features including periungual fibromas, shagreen plaques, oral papillomatosis, ash leaf hypomelanotic macules, skin fibromas, and café au lait spots. Adenoma sebaceum are 1-3 mm, yellowish, red discrete, waxy papules that are distributed symmetrically over the cheeks, nose, and forehead. Histologically, these are angiofibromas. Congenital hypomelanotic macules are found in 85% of TS patients which may be detected at birth in most patients. They may be shaped like an ash leaf, but linear and confetti-type white macules may be present. The hypomelanotic macules are an indication for a skull x-ray evaluation to search for calcified intracranial nodules. These are hamartomatous proliferations of glial and neuronal tissue produce potato-like nodules or brain stones in the cortex leading to seizures.

Checking levels of cortisol (choice A) and DHEAS/ testosterone (choice B) is incorrect because this patient does not show other signs of endocrine abnormalities (i.e., hypertrichosis and enlarged external genitalia).

Prescribing minocycline (choice C) and benzoyl peroxide and erythromycin (choice D) is incorrect, because these treatments are aimed at treating acne lesions.

A mentally challenged 18-year-old man who had been calmly walking down a street suddenly cried out, fell to the ground, and started to have jerky movements of his right arm and leg accompanied by a twitching of the face. Passersby stopped to help and noticed that he was frothing from the mouth, had wet his trousers, and bitten his tongue. The para- medics were called, and they swiftly transported him to the emergency room. The attending physician
noted he had some small firm swellings around the nose, as well as freckle-like dark spots on his face. The clinical condition affecting this patient can result in the development of which one of the following conditions?

A. Oligodendroglioma
B. Melanoma
C. Renal failure
D. Peripheral vascular disease 
E. Hepatic failure

The answer is C. This patient is suffering from tuberous sclerosis complex (TSC), an autosomal dominant disease with variable penetrance, in which there is a genetic mutation involving two genes, TSC1 and TSC2; these turn on two tumor-suppressor proteins, tuberin and hamartin, located on chromosome 16 and 9, respectively. As a result, tumors, most often benign, and cysts may develop. The disease affects various organs with variable severity. The features of this syndrome include mental retardation, seizures, and adenoma sebaceum, characterized by firm nodules on the face in a butterfly distribution. Patients with this disease may have renal cysts (angiomy- olipomas) that could lead to hematuria, and renal failure could supervene (choice C is correct).

Patients with this disorder can develop tubers on the cortex (hence the name); these are subependymal nodules of glial or neuronal origin, as well as subependymal giant cell astrocytomas that can block the fora- men of Munro. This may lead to acute hydrocephalus, with a tragic outcome if not recognized and treated; however, since oligodendroglioma (choice A) are tumors in their own right, they are not expected to be present in patients suffering from TSC. Melanomas do not present with café au lait spots on the face, nor is there any reason to suspect that this patient has a melanoma (choice B). Other skin manifestations of the disease may include the Shagreen patch, wherein the skin has the texture of leather (often seen on the lower back or over the back of the neck), and “ash leaf spots,” which are hypomelanotic patches that can occur in various parts of the body. Peripheral vascular disease (choice D) is not a manifestation of this disease, although these patients can develop cardiovascular problems such as rhabdomyomas, cardiac murmurs, arrhythmias, and cardiac failure in early infancy and childhood, and sometimes during their adult years. Hepatic failure (choice E) is not a feature of this disease.
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Respiratory Distress Syndrome   
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Respiratory distress syndrome is caused by pulmonary surfactant deficiency in the lungs of neonates, most commonly in those born at < 37 wk gestation. Risk increases with degree of prematurity. Symptoms and signs include grunting respirations, use of accessory muscles, and nasal flaring appearing soon after birth. Diagnosis is clinical; prenatal risk can be assessed with tests of fetal lung maturity. Treatment is surfactant therapy and supportive care.

Surfactant is not produced in adequate amounts until relatively late in gestation (34 to 36 wk); thus, risk of respiratory distress syndrome (RDS) increases with greater prematurity. Other risk factors include multifetal pregnancies, maternal diabetes, and being male and white.

Risk decreases with fetal growth restriction, preeclampsia or eclampsia, maternal hypertension, prolonged rupture of membranes, and maternal corticosteroid use.

Pulmonary surfactant is a mixture of phospholipids and lipoproteins secreted by type II pneumocytes. It diminishes the surface tension of the water film that lines alveoli, thereby decreasing the tendency of alveoli to collapse and the work required to inflate them.

With surfactant deficiency, a greater pressure is needed to open the alveoli. Without adequate airway pressure, the lungs become diffusely atelectatic, triggering inflammation and pulmonary edema. Because blood passing through the atelectatic portions of lung is not oxygenated (forming a right-to-left intrapulmonary shunt), the infant becomes hypoxemic. Lung compliance is decreased, thereby increasing the work of breathing. In severe cases, the diaphragm and intercostal muscles fatigue, and CO 2 retention and respiratory acidosis develop.

Symptoms and Signs

Symptoms and signs include rapid, labored, grunting respirations appearing immediately or within a few hours after delivery, with suprasternal and substernal retractions and flaring of the nasal alae. As atelectasis and respiratory failure progress, symptoms worsen, with cyanosis, lethargy, irregular breathing, and apnea.

Neonates weighing < 1000 g may have lungs so stiff that they are unable to initiate or sustain respirations in the delivery room.

On examination, breath sounds are decreased. Peripheral pulses may be decreased with peripheral extremity edema and decreased urine output.

• Clinical evaluation
• ABG (hypoxemia and hypercapnia)
• Chest x-ray
• Blood, CSF, and tracheal aspirate cultures

Diagnosis is by clinical presentation, including recognition of risk factors; ABGs showing hypoxemia and hypercapnia; and chest x-ray. Chest x-ray shows diffuse atelectasis classically described as having a ground-glass appearance with visible air bronchograms; appearance correlates loosely with clinical severity.


RDS can be anticipated prenatally using tests of fetal lung maturity, which are done on amniotic fluid obtained by amniocentesis or collected from the vagina (if membranes have ruptured) and which can help determine the optimal timing of delivery. These are indicated for elective deliveries before 39 wk when fetal heart tones, human chorionic gonadotropin levels, and ultrasound measurements cannot confirm gestational age and for nonelective deliveries between 34 wk and 36 wk.

Amniotic fluid tests include the:
• Lecithin/sphingomyelin ratio
• Foam stability index test (the more surfactant in amniotic fluid, the greater the stability of the foam that forms when the fluid is combined with ethanol and shaken)
• Surfactant/albumin ratio

Risk of RDS is low when lecithin/sphingomyelin ratio is > 2, phosphatidyl glycerol is present, foam stability index = 47, or surfactant/albumin ratio is > 55 mg/g.

• Surfactant
• Supplementary O 2 as needed
• Mechanical ventilation as needed

Prognosis with treatment is excellent; mortality is < 10%. With adequate ventilatory support alone, surfactant production eventually begins, and once production begins, RDS resolves within 4 or 5 days. However, in the meantime, severe hypoxemia can result in multiple organ failure and death.

Specific treatment is intratracheal surfactant therapy. This therapy requires endotracheal intubation, which also may be necessary to achieve adequate ventilation and oxygenation. Less premature infants (those> 1 kg) and those with lower O 2 requirements (fraction of inspired O 2 [F io 2 ] < 40 to 50%) may respond well to supplemental O 2 alone or to treatment with nasal continuous positive airway pressure. A treatment strategy of early (within 20 to 30 min after birth) surfactant therapy is associated with significant decrease in duration of mechanical ventilation, lesser incidence of air leak syndromes, and lower incidence of bronchopulmonary dysplasia.

Surfactant hastens recovery and decreases risk of pneumothorax, interstitial emphysema, intraventricular hemorrhage, bronchopulmonary dysplasia, and neonatal mortality in the hospital and at 1 yr. However, neonates who receive surfactant for established RDS have an increased risk of apnea of prematurity.

Lung compliance can improve rapidly after therapy. The ventilator peak inspiratory pressure may need to be lowered rapidly to reduce risk of a pulmonary air leak. Other ventilator parameters (eg, F io 2 , rate) also may need to be reduced.


When a fetus must be delivered between 24 wk and 34 wk, giving the mother 2 doses of betamethasone 12 mg IM 24 h apart or 4 doses of dexamethasone 6 mg IV or IM q 12 h at least 48 h before delivery induces fetal surfactant production and reduces the risk of RDS or decreases its severity.

Prophylactic intratracheal surfactant therapy given to neonates that are at high risk of developing RDS (infants < 30 wk completed gestation especially in absence of antenatal corticosteroid exposure) has been shown to decrease risk of neonatal death and certain forms of pulmonary morbidity (eg, pneumothorax).

Key Points
• Respiratory distress syndrome (RDS) is caused by pulmonary surfactant deficiency, which typically occurs only in neonates born at < 37 wk gestation; deficiency is worse with increasing prematurity.
• With surfactant deficiency, alveoli close or fail to open, and the lungs become diffusely atelectatic, triggering inflammation and pulmonary edema.
• In addition to causing respiratory insufficiency, RDS increases risk of intraventricular hemorrhage, tension pneumothorax, bronchopulmonary dysplasia, sepsis, and death.
• Diagnose clinically and with chest x-ray; exclude pneumonia and sepsis by appropriate cultures.
• If premature delivery is anticipated, assess lung maturity by testing amniotic fluid for lecithin/sphingomyelin ratio, foam stability, or the surfactant/albumin ratio.
• Treat with intratracheal surfactant and give respiratory support as needed.
• Give the mother several doses of a parenteral corticosteroid (betamethasone, dexamethasone) if she must deliver between 24 wk and 34 wk gestation; corticosteroids induce fetal surfactant production and reduce the risk and/or severity of RDS.


While in the hospital discharging a patient, you are notified that another one of your patients, a 32-year-old woman who is at 28-weeks gestation, is in labor on the delivery floor. By the time you arrive at the correct room, the baby has already been delivered by cesarean section and transferred to the neonatal intensive care unit. The apgar scores were 7 at 1 minute and 8 at 5 minutes. After evaluating the mother, you go to the neonatal intensive care unit to see the baby. When you arrive, you notice that she has nasal flaring, subcostal and intercostal retractions, cyanosis, and tachypnea. The most appropriate next diagnostic step is to

A. call for a pediatric cardiology consult
B. obtain an umbilical artery blood gas
C. obtain sputum samples for cytology
D. obtain vaginal cultures from the mother
E. order a chest x-ray

The correct answer is E. This baby born at 28 weeks is at a very high risk for respiratory distress syndrome due to insufficient surfactant levels. The decreased surfactant levels lead to a decrease in lung compliance and alveolar hypoventilation and ventilation-perfusion imbalance. Within an hour of birth, infants often have nasal flaring, subcostal and intercostal retractions, cyanosis, expiratory grunting, and tachypnea. A chest x-ray will show diffuse reticulogranular pattern in both lung fields with superimposed air bronchograms. Other possible causes for this patient's symptoms are pneumonia, hypoglycemia, anemia, polycythemia, hypothermia, or metabolic acidosis.

A pediatric cardiology consult (choice A) is not indicated at this time. It seems as if this patient has a respiratory process and therefore needs a chest x-ray. If the x-ray is negative, a cardiology consult may be indicated.

An umbilical artery blood gas (choice B) should be obtained after the chest x-ray is taken. The case states that the baby is cyanotic and so you would suspect that the ABG will show hypoxemia. It will not be very helpful in determining the exact cause for her symptoms.

Since it is very unlikely that this patient's symptoms are caused by a malignant process, sputum samples (choice C) are not indicated at this time. A chest x-ray will most likely be helpful in determining the cause of her symptoms.

Since this patient's symptoms can be caused by pneumonia or another infectious process, vaginal cultures from the mother should be taken (choice D). However, a chest x-ray of the baby will hopefully provide rapid findings and should therefore be done first.

In preparation for delivery, an amniocentesis is performed. Which of the following parameters is most useful in predicting lung maturity of the infant?

A. Lecithin/sphingomyelin (L/S) ratio 􏰃2:1 
B. L/S ratio 􏰂 1:4
C. L/S ratio 􏰂 4:1
D. Type I alveolar cells in the amniotic fluid 
E, Type II alveolar cells in the amniotic fluid

Answer: C. Amniocentesis may help predict lung maturity. Surfactant production generally begins during weeks 26 to 28, the terminal sac phase of lung development. At this time, the surface area of the lungs increases progressively. Surfactant is needed to decrease alveolar surface tension and increase lung compliance, preventing alveolar collapse at the end of expiration. The lecithin/sphingomyelin ratio (L/S) is predictive of lung maturity. An L/S ratio of more than 2:1 generally indicates lung maturity. It would be highly unlikely that an infant delivered at 28 weeks would have such a ratio.

A 25-year-old woman, who is G2P1, experiences frequent contractions accompanied by cervical effacement at 26 weeks of pregnancy. The cervix is not dilated. You have many concerns, including the lack of pulmonary development. Which of the following measures might hasten lung development?

A. Ritodrine hydrochloride 
B. Betamethasone
C. Terbutaline sulfate
D. Indomethacin
E. Magnesium sulfate

Answer: B. At 26 weeks of gestation, the fetal lungs are poorly developed. Even at 32 weeks of gestation, the production of surfactant is still poor. This patient is in preterm labor, which is defined as regular uterine contractions with cervical change between 20 and 36 weeks of pregnancy. The administration of a steroid, such as betamethasone, hastens pulmonary maturity and reduces the incidence and mortality from respiratory distress syndrome. The 􏰄2-agonists ritodrine and terbutaline are used to inhibit uterine contractions in preterm labor. Indomethacin is used occasionally in preterm labor because it inhibits prostaglandin production, which causes uterine contractions. If indomethacin is used after 34 weeks, it can cause premature closure of the ductus arteriosus. Magnesium sulfate competes with calcium at the neuromuscular junction to inhibit uterine contractions as well.

A decision is made to deliver the infant. A neonatologist is called to attend the delivery secondary to the prematurity of the infant. A cesarean section is performed, and the infant is successfully delivered. However, the infant is in severe respiratory distress and is immediately placed in 100% oxygen. An arterial blood gas is obtained with a pH of 7.2, a PO2 of 50 mm Hg, and a PCO2 of 65 mm Hg. The next appropriate step in the management of this infant is

A. intubation with mechanical ventilation
B. exogenous surfactant instillation
C. intravenous hydration
D. intubation with mechanical ventilation and exogenous surfactant instillation
E. intubation with mechanical ventilation and intravenous hydration

Answer: D. The infant is in respiratory distress with a respiratory acidosis and hypoxemia. Emergent intubation, ventilation, and instillation of exogenous surfactant are required. In the absence of hypovolemia, intravenous hydration is not necessary acutely. In fact, there is a small risk of causing an intraventricular hemorrhage in such a premature infant by the overly aggressive introduction of intravenous fluids.
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