Internal Medicine

Internal Medicine

by Bruce F. Scharschmidt
Pub. Date:
Cambridge University Press


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Internal Medicine

Cambridge Pocket Clinician / Internal Medicine is designed to provide the busy clinician with precisely the information needed where and when it is needed. The Associate Editors and contributors are internationally recognized authorities, and they have organized the content specifically so as to convey the essentials necessary for diagnosis, differential diagnosis, management, treatment and follow-up. Over 600 diseases and conditions are covered in detail. Cambridge Pocket Clinician / Internal Medicine can be counted on as an essential resource, particularly in this current era of shortened physician patient encounters and the need for rapid clinical decision-making.

Product Details

ISBN-13: 9780521709408
Publisher: Cambridge University Press
Publication date: 09/30/2007
Series: Cambridge Pocket Clinicians Series
Pages: 1500
Product dimensions: 5.98(w) x 8.98(h) x 2.28(d)

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Internal medicine
Cambridge University Press
978-0-521-70940-8 - Internal Medicine - Edited by Bruce F. Scharschmidt




■ Male:female ratio is 4:1

■ 5–10% of males over 65 years of age have AAA

■ High incidence in patients with peripheral arterial aneurysm (popliteal, femoral)

■ Ruptured AAA – clinical suspicion

  ➢ elderly male with severe back or abdominal pain

  ➢ may radiate to groin.

Signs & Symptoms

■ Most are asymptomatic and found on other imaging studies

■ pulsatile abdominal mass in less than 30% of patients with significant AAA

■ Tender abdominal mass is suggestive of symptomatic aneurysm

■ examine for associated peripheral aneurysms (femoral, popliteal)

■ Unusual presentations:

  ➢ atheroembolism to lower extremities

  ➢ thrombosis (sudden severe ischemia of legs)

  ➢ high outputCHF from aortocaval fistula

  ➢ GI bleeding from primary aorto-enteric fistula

■ Ruptured AAA

  ➢ Pulsatile mass + hypotension

  ➢ abdominal/back/groin pain + hypotension



■ None


■ Ultrasound for screening

■ CT scan is best test for aneurysms being considered for repair

■ Defines : associated iliac aneurysms, eligibility for endovascular repair, possible suprarenal extension

■ Conventional MRI has no advantage over CT for AAA

■ Angiography is not used for diagnosis (can miss AAA due to normal lumen)

■ Angiography (contrast or MR) indicated preoperatively in patients with:

  ➢ clinical suspicion of concurrent renal artery stenosis (severe hypertension, elevated creatinine)

  ➢ mesenteric occlusive disease (post-prandial pain)

  ➢ significant lower extremity occlusive disease (claudication + ankle/ brachial index<0.7).

■ Ruptured AAA: if diagnosis is unclear (no mass):

   ➢ Emergency ultrasound

   • helpful only if aorta is clearly seen and completely normal

   • often not helpful due to bowel gas and patient discomfort

   • cannot rule out a leak from AAA

  ➢ CT scan

   • Best test when diagnosis of AAA is unclear

   • Emergency non-contrast scan of abdomen

   • Intravenous contrast increases post-op renal failure and is not needed to see AAA or leak

   • Oral contrast not required


Ruptured AAA

■ most common misdiagnosis is kidney stone

■ second most common is musculoskeletal back pain; high suspicion of AAA with new onset or change in chronic back pain

■ other:

  ➢ appendicitis (associated GI symptoms)

  ➢ diverticulitis (fevers, GI symptoms, focal left sided tenderness)

  ➢ aortic dissection (ripping pain, extends into chest and upper back)

  ➢ incarcerated hernia (physical exam, CT scan if exam inconclusive)


What to Do First

■ Emergent (immediate) operation in patients with abdominal pain and hypotension due to ruptured AAA

■ Emergent non-contrast CT scan in patients with symptoms suggestive of ruptured AAA

General Measures

■ Rule out ruptured AAA first in all patients with suggestive symptoms, as it is the most rapidly lethal diagnosis if missed

■ Risk/benefit ratio of elective repair is contingent upon low operative mortality (less than 5%)



■ Most patients

  ➢ Elective repair if diameter in any orientation is 5 to 5.5 cm

  ➢ Repair if serial scans (either ultrasound or CT) demonstrate rapid growth (> 1 cm/year) or saccular growth

  ➢ Urgent repair in patients with symptoms (tenderness)

  ➢ Repair associated lesions (renal, visceral or peripheral occlusive disease) concurrently if indicated

■ Poor-risk patients

  ➢ consider endovascular repair

  ➢ discuss with patient/family outcome if not repaired

  ➢ (Risk of rupture is 2–3% per year at 5 cm, and may not be significant relative to other co-morbidities)

Treatment Options

■ Operative repair

  ➢ Most durable treatment

  ➢ Little difference between transperitoneal and retroperitoneal repairs

  ➢ Intraoperative pulmonary artery catheters in patients with poor ejection fraction or CHF

Side Effects and Contraindications

■ Operative repair

  ➢ Perioperative mortality should be less than 5%

  ➢ Complications

   • Myocardial infarction:

   • Clinical indices (Goldman criteria, Eagle criteria) are predictive of risk, but persantine thallium scanning is not.

   • MI after elective repair is rarely fatal

  ➢ Ischemic colitis

   • Seen more often after ruptured AAA with hypotension

  ➢ Renal failure

   • Seen after repair of ruptured and suprarenal AAA. Associated with high mortality (50%)

■ Contraindications

  ➢ Expected survival less than 50% at 5 years due to associated cardiovascular disease

    • Endovascular Repair

■ Lower mortality and morbidity than open repair

■ Less durable than standard repair

■ Absolute Contraindications

  ➢ Bilateral common iliac artery aneurysms

  ➢ Pararenal or suprarenal aneurysm

  ➢ Angulation, thrombus or dilation of infrarenal neck

  ➢ Iliac occlusion or stenosis precluding transfemoral access

■ Relative contraindications

  ➢ Long term anticoagulation (higher risk of endoleak [see below])

  ➢ Associated occlusive disease requiring treatment

Specific Complications

■ Endoleak

  ➢ Persistent arterial flow in aneurysm sac due to: failure of device to seal to arterial wall (Type I), back flow from branch vessel (Type Ⅲ) or leak through graft material (Type Ⅲ)

■ Post-implant fever

  ➢ Occurs 12–48 hours after implant; not due to infection


During Treatment

■ Follow AAA less than 5 cm with serial ultrasound or CT scans q6–12 months, or more frequently if there is rapid change in size


■ Patients undergoing endovascular repair require lifelong yearly CT scan to monitor position and seal of device



■ Myocardial Infarction

■ Renal failure

  ➢ Poor prognosis (50% mortality). Treatment is supportive. Usually resolves (ATN)

■ Ischemic colitis

  ➢ Diagnose by bedside sigmoidoscopy. Colectomy for full-thickness ischemia; serial endoscopy for mucosal ischemia which often resolves. May cause late ischemic strictures.

■ Endoleak (seen only after endovascular repair)

  ➢ Diagnosed on post-op CT scan or angiogram. Treatment is usually endovascular

■ Graft Infection

  ➢ Can occur after either open or endovascular repair. Symptoms: persistent fever or aorto-enteric fistula (upper GI bleeding). Diagnosis: CT scan. Treatment: graft excision and extra-anatomic bypass. Mortality: 50%.


■ Ruptured AAA

  ➢ Most die en route to hospital or on arrival

  ➢ 50% of those undergoing surgery survive

  ➢ Preoperative predictors of poor survival:

    • age > 80

   • preoperative hypotension

   • elevated creatinine preop or postop renal failure

■ Elective Repair

  ➢ Perioperative mortality approximates 5%

■ Endovascular Repair

  ➢ Requires life-long follow-up for late complications

   • Late onset endoleak:

   • Graft migration or disruption

  ➢ Late complications

   • Graft infection (1%)

   • Secondary aorto-enteric fistula




Risk Factors

■ Recent abdominal surgery

■ Penetrating or blunt abdominal trauma

■ Perforation of appendix or colonic diverticulum

■ Perforation associated w/ intraabdominal malignancy

■ Crohn disease

■ Chronic diseases, eg, cirrhosis, renal failure

■ Drugs, eg, corticosteroids, chemotherapy

■ Prior radiotherapy


■ High spiking fevers w/ chills

■ Abdominal pain

■ Nausea & vomiting

■ Hiccups

■ Chest pain

■ Dyspnea

■ Shoulder pain

Signs & Symptoms

■ Tachycardia

■ Abdominal tenderness

■ Ileus

■ Pleural effusion

■ Basilar rales


Basic Blood Tests

■ Leukocytosis w/ left shift

■ Anemia

■ Nonspecific elevation of bilirubin & liver enzymes

Specific Diagnostic Tests

■ Positive blood cultures

■ Positive cultures from aspiration of abscess

■ Most common aerobes: E coli & Enterococcus

■ Most common anaerobes: Bacteroides


■ Plain abdominal & chest films: air-fluid levels in area of abscess; elevation of right diaphragm in subphrenic abscess

■ Gallium scan: useful for smaller abscess not well seen on imaging

CT: imaging modality of choice for identification of abscess; also allows aspiration for culture

US: less sensitive for abdominal abscesses

■ Charcoal or methylene blue: oral administration with detection in drainage from fistula


■ Necrotic tumors


What to Do First

■ Complete diagnostic studies, particularly imaging, for localization & aspiration

General Measures

■ Initiate general supportive care: fluid & electrolyte replacement, establish feeding (TPN if fistula present), oxygenation if needed

■ Swan-Ganz catheter, mechanical ventilation &/or vasopressors if unstable


■ Adequate drainage of abscess either percutaneously or by surgery

■ Surgery indicated if pt fails to respond to percutaneous drainage in 1–2 d

■ Establish adequate drainage of enterocutaneous fistulas, eg, open recent surgical excision, use of percutaneous catheters

■ Surgery for complex fistulas or failure to resolve w/ external drainage & TPN

■ Antibiotics: broad spectrum initially, & then based on culture results


■ Frequent clinical evaluation early after drainage

■ Serial imaging when treated w/ catheter drainage to confirm catheter w/i abscess & abscess closed



■ Multiorgan failure leading to death

■ Recurrent abscess

■ Fistula formation

■ Bowel obstruction

■ Pneumonia

■ Pleural effusion


■ Good w/ adequate drainage & response to antibiotic therapy

Acanthosis Nigricans




■ A cutaneous marker of insulin resistance states

■ Other etiologies: hereditary, endocrine disorders, obesity, drugs, and malignancy

■ Seen in blacks > Hispanics > whites

■ Five types:

  ➢ Type Ⅰ (Familial)

   • Exceedingly rare

   • Autosomal dominant

   • Present at birth or develops during childhood

   • Worsens at puberty

   • Not associated with an internal cancer

  ➢ Type Ⅱ (Benign AN)

   • Associated with various endocrine disorders

   • Examples include acromegaly, gigantism, Stein-Leventhal syn-drome, Cushing’s, diabetes mellitus, hypothyroidism, Addison’s disease, hyperandrogenic states, and hypogonadal syndromes

  ➢ Type Ⅲ (formerly called Pseudo-AN; however, this probably is the result of an endocrinopathy, namely insulin resistance)

   • Most common form

   • Associated with obesity and insulin resistance states

   • Not associated with malignancy

  ➢ Type IV (Drug-induced):

   • Nicotinic acid, niacinamide, diethylstilbestrol, triazineate, oral contraceptives, testosterone, topical fusidic acid, and glucocorticoids

   • Seen in 10% of renal transplant patients

  ➢ Type Ⅴ (Associated with malignancy):

   • Rare

   • Most often in adults

   • Highly suspected if occurs in non-obese male

   • Tends to be more widespread and involve mucosal surfaces

   • Precedes 18%, accompanies 60%, or follows 22% the internal malignancy

   • Most often associated with adenocarcinoma of gastrointestinal tract (60% stomach)

   • Also associated with lung and breast adenocarcinoma

   • Other cancers also seen

Signs & Symptoms

■ Often asymptomatic; skin looks “dirty”

■ Velvety brown thickening of skin on intertriginous surfaces, most commonly the axilla, the neck

■ Other sites: genitalia, knuckles, lips, submammary area, umbilicus, eyelids, and conjunctiva


■ Use history and physical as guide to appropriate workup

Basic Tests:

■ Check blood glucose and possibly an insulin level

Other Tests:

■ Exclude malignancy in non-obese patients with no obvious cause

■ Screen for malignancy as appropriate for patients age, risk factors, and symptoms

■ Screen for endocrinopathy if suspected




■ Depends on cause:

   ➢ Weight loss if obese

  ➢ Treat underlying endocrinopathy

  ➢ Discontinue offending drug

■ Topical urea, lactic acid, tretinoin, and oral etretinate used with varied success


Urea-containing products may give symptomatic relief.


■ Varies dependent upon the association with an underlying disorder or disease


■ Depends on underlying cause

■ Obesity related AN improves with weight loss

■ Endocrinopathy associated AN improves with treatment of underlying disease

■ Removal of malignancy may be followed by regression of AN


Alfred L. Knable, MD


■ May exist transiently during neonatal period

■ Commonly begins during early puberty with increased activity throughout the teens with spontaneous resolution thereafter (strong genetic influence recognized)

■ May begin at or persist into later ages

■ May result from exposure to various oils, greases, etc. found in cosmetics, pomades, or industry

■ May result from or be exacerbated by hormones - Polycystic ovary disease, insulin resistance, hyperandrogenism, Cushing’s disease

■ Complication of various drugs: corticosteroids, lithium, iodide/ bromide, anticonvulsants

Signs & Symptoms

■ Primary lesion = microcomedo (clinically unrecognizable = microscopic plugging of pilosebaceous unit)

■ First clinically recognizable lesions are open comedones (“blackheads”) and/or closed comedones (“whiteheads”)

■ Earliest stages most common on forehead and across nose and chin

■ Later stages of development include inflammatory papules (1–5 mm) and pustules

■ Most advanced lesions are cystic and/or nodular (>=5 mm) with a predilection for lateral cheeks, chin and in more severe cases the chest and upper back (acne conglobata)

■ Evaluate for signs of endocrinologic disease – hirsutism, striae, Cushingoid facies


■ Laboratory – routine: none except when indicated for specific therapies

■ Screening. Woman with severe or recalcitrant acne (or the onset or recurrence of acne beyond their late twenties) should have at least a measurement of their free testosterone and dehydroepiandrosterone sulfate levels to consider polycystic ovarian disease or Stein-Leventhal syndrome.


■ Pityrosporum or bacterial folliculitis more likely to occur on trunk, buttocks, and proximal extremities with follicular-based papules or pustules

■ Acne keloidalis nuchae occurs as firm 2- to 5-mm papules on the occiput of African-American men

■ Pseudofolliculitis barbae occurs as firm papules and occasionally pustules to beard areas of African-American men

■ Hidradenitis suppurativa occurs within the axillae, under the breasts and the inguinal areas with larger cysts and sinus tract formation.

■ Rosacea – more central facial and/or perioral, more common in adults, lack of comedones

© Cambridge University Press

Table of Contents

1. Abdominal aortic aneurysm (AAA); 2. Abscesses and fistulas; 3. Acanthosis nigricans; 4. Acne; 5. Acromegaly; 6. Actinic keratosis; 7. Acute acalculous cholecystitis; 8. Acute bacterial meningitis; 9. Acute fatty liver of pregnancy; 10. Acute heart failure; 11. Acute lymphoblastic leukemia; 12. Acute myeloblastic leukemia; 13. Acute myocarditides; 14. Acute pancreatitis; 15. Acute pericarditis; 16. Acute renal failure; 17. Acute respiratory acidosis; 18. Acute respiratory alkalosis; 19. Acute respiratory failure/monitoring; 20. Adenocarcinoma of the ampulla of vater; 21. Adenovirus; 22. Adrenal insufficiency ; 23. Adrenal tumors; 24. Adult optic neuropathies; 25. Age related maculopathy; 26. Air embolus; 27. Alcohol abuse, dependence, and withdrawal; 28. Alcoholic liver disease (ALD); 29. Allergic rhinitis; 30. Alopecia; 31. Alpha-1-antitrypsin; 32. Alzheimer's disease; 33. Amaurosis fugax; 34. Amblyopia; 35. Amebiasis; 36. Amebic liver abscess; 37. Amyloidosis; 38. Amyotrophic lateral sclerosis (ALS); 39. Analgesic nephropathy and NSAID-induced ARF; 40. Anaphylaxis; 41. Anemias secondary to systemic disease; 42. Anisakiasis; 43. Anorectal tumors; 44. Anorexia nervosa; 45. Antibiotic-associated and pseudomembranous colitis; 46. Antiphospholipid antibodies; 47. Aortic coarctation; 48. Aortic dissection; 49. Aortic insufficiency (AI); 50. Aortitis; 51. Aphasia; 52. Aplastic anemia; 53. Apparent mineralocorticoid excess; 54. Appendicitis; 55. Arterial embolus; 56. Ascariasis; 57. Ascites; 58. Aspergillosis; 59. Asthma; 60. Atelectasis; 61. Atherosclerotic occlusive disease; 62. Atopic dermatitis (dermatitis, atopic); 63. Atrial fibrillation (AF); 64. Atrial flutter; 65. Atrial premature complexes; 66. Atrial septal defect (ASD); 67. Atrial tachycardia (AT); 68. Atrioventricular block; 69. Autoimmune hepatitis (AIH); 70. Autonomic dysfunction; 71. Autosomal dominant polycystic renal disease; 72. Autosomal recessive polycystic renal disease; 73. Av reentrant tachycardia (AVRT); 74. Av-nodal reentrant tachycardia (AVNRT); 75. Back or neck pain; 76. Bacterial arthritis; 77. Bacterial pneumonia; 78. Balanitis; 79. Bartter's syndrome; 80. Bell's palsy; 81. Benign disorders of the rectum and anus; 82. Benign prostatic hyperplasia; 83. Benign tumors of the liver; 84. Biliary tract motility disorders; 85. Bladder tumors; 86. Blastocystis hominis infection; 87. Blastomyces dermatitidis; 88. Blepharitis (lid infection); 89. Brain abscess; 90. Brain death; 91. Bronchiectasis; 92. Bronchiolitis; 93. Bronchitis, acute; 94. Budd-chiari syndrome; 95. Buerger's disease; 96. Bulimia nervosa; 97. Bullous pemphigoid; 98. Bullous pemphigoid; 99. Candidiasis; 100. Candidiasis: oral; 101. Carcinoid; 102. Cardiac arrest; 103. Cardiac trauma; 104. Cardiac tumors; 105. Cat scratch disease; 106. Cecal volvulus; 107. Celiac sprue and malabsorption; 108. Cellulitis; 109. Cerebrovascular disease and stroke; 110. Cervical spine disorders; 111. Chediak higashi syndrome; 112. Cheilitis; 113. Cholangiocarcinoma; 114. Choledochal cysts; 115. Cholestasis; 116. Cholestasis of pregnancy; 117. Chordae tendineae rupture; 118. Chromium deficiency; 119. Chronic acalculous cholecystitis; 120. Chronic bundle branch block and hemi-blocks; 121. Chronic coronary artery disease (CAD); 122. Chronic heart failure; 123. Chronic lymphocytic leukemia; 124. Chronic myelogenous leukemia; 125. Chronic obstructive pulmonary disease (COPD); 126. Chronic pancreatitis; 127. Chronic respiratory acidosis; 128. Chronic respiratory alkalosis; 129. Chronic respiratory failure; 130. Clostridium infections (other than tetanus, botulism and c. Difficile diseases); 131. Cluster headache; 132. Coccidioides immitis; 133. Colon polyps and tumors; 134. Coma; 135. Complications of human immunodeficiency virus type 1 (HIV-1) infection; 136. Condyloma acuminata; 137. Confusion and delirium; 138

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