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First_Aid_Step2. In patients with oliguria, the FeNa can help identify prerenal failure and distinguish it from intrinsic renal disease. Obtain a renal biopsy only when the cause of intrinsic renal disease is unclear. Balance ﬂuids and electrolytes; avoid nephrotoxic drugs. In acute or allergic interstitial nephritis, adjust or discontinue offending medications. Dialyze if indicated (see the mnemonic AEIOU) using hemodialysis. Peritoneal dialysis should be considered only for long-term dialysis patients or for patients who are not hemodynamically stable. Metabolic acidosis; hyperkalemia leading to arrhythmias. Hypertension (from renin hypersecretion). Volume overload leading to CHF and pulmonary edema. Chronic kidney disease may result, requiring dialysis to prevent the buildup of K+, H+, phosphate, and toxic metabolites. Ingestions (salicylates, theophylline, methanol, barbiturates, lithium, ethylene glycol)


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First_Aid_Step2. Ingestions (salicylates, theophylline, methanol, barbiturates, lithium, ethylene glycol) Uremic symptoms (pericarditis, encephalopathy, bleeding, nausea, pruritus, myoclonus) Most commonly due to diabetes mellitus (DM), hypertension, and glomerulonephritis. Another commonly tested etiology is polycystic kidney disease (the autosomal-dominant form is more common and is adult onset; the autosomalrecessive form is seen in children). Generally asymptomatic until GFR < 30, but patients gradually experience the signs and symptoms of uremia (anorexia, nausea, vomiting, uremic pericarditis, “uremic frost,” delirium, seizures, coma). Common metabolic derangements include the following: Azotemia (↑ BUN and creatinine). Fluid retention (hypertension, edema, CHF, pulmonary edema). Metabolic acidosis. Hyperkalemia. Anemia of chronic disease (↓ erythropoietin production).


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First_Aid_Step2. Azotemia (↑ BUN and creatinine). Fluid retention (hypertension, edema, CHF, pulmonary edema). Metabolic acidosis. Hyperkalemia. Anemia of chronic disease (↓ erythropoietin production). Hypocalcemia, hyperphosphatemia (↓ phosphate excretion; impaired vitamin D production leading to renal osteodystrophy). ACEIs/ARBs and hypertension control have been shown to ↓ the progression of CKD. Additional pharmacotherapy is as follows: Erythropoietin analogs for anemia of chronic disease. Fluid restriction; low Na+/K+/phosphate intake. Oral phosphate binders and calcitriol (1,25-OH vitamin D) for renal osteodystrophy. Renal replacement therapy includes hemodialysis, peritoneal dialysis, and renal transplantation. Table 2.16-5 and Figure 2.16-3 summarize the mechanisms of action and side effects of commonly used diuretics. T AB LE 2.1 6-5. Mechanism of Action and Side Effects of Diuretics


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First_Aid_Step2. Carbonic anhydrase inhibitors Acetazolamide Proximal convoluted tubule. Inhibit carbonic anhydrase, ↑ H+ reabsorption, block Na+/ H+ exchange. Hyperchloremic metabolic acidosis, sulfa allergy. Osmotic agents Mannitol, urea Entire tubule. ↑ tubular fuid osmolarity. Pulmonary edema due to CHF and anuria. Loop agents Furosemide, ethacrynic acid, bumetanide, torsemide Ascending loop of Henle. Inhibit Na+/K+/2Cl– transporter. Water loss, metabolic alkalosis, ↓ K+, ↓Ca2+, ototoxicity, sulfa allergy (except ethacrynic acid, hyperuricemia). Thiazide agents HCTZ, chlorothiazide Distal convoluted tubule. Inhibit Na+/Cl– transporter. Water loss, metabolic alkalosis, ↓Na+, ↓ K+, ↑ glucose, ↑Ca2+, ↑ uric acid, sulfa allergy, pancreatitis. K+-sparing agents Spironolactone, triamterene, amiloride Cortical collecting tubule. Aldosterone receptor antagonist (spironolactone); block sodium channel (triamterene, amiloride). Metabolic acidosis; ↑ K+; antiandrogenic effects, including gynecomastia


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First_Aid_Step2. Cortical collecting tubule. Aldosterone receptor antagonist (spironolactone); block sodium channel (triamterene, amiloride). Metabolic acidosis; ↑ K+; antiandrogenic effects, including gynecomastia (spironolactone).


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First_Aid_Step2. Glomerulusconvoluted tubule Proximal straight tubule 1 Cortex Outer medulla Diuretics 1 Acetazolamide 2 Osmotic agents (mannitol) 3 Loop agents (e.g., furosemide) 4 Thiazides5 Aldosterone antagonists6 ADH antagonists2 2 2 3 4 5 6 Thin descending limbH2O H2O H2O (+ADH) Inner medulla Loop of Henle Thin ascending limbThick ascending limbNa+ K+ K+ 2Cl−Ca2+ Mg2+ tubule(+PTH) (+aldosterone) ? 4 F IGU R E 2.1 6-3. Overview of diuretics. (Reproduced, with permission, from Katzung BG. Basic & Clinical Pharmacology, 10th ed. New York: McGraw-Hill, 2007: Fig. 15-1.) A disorder of glomerular inﬂammation, also called glomerulonephritis. Proteinuria may be present but is usually < 1.5 g/day. Causes are summarized in Table 2.16-6. The classic findings are oliguria, macroscopic/microscopic hematuria (teaor cola-colored urine), hypertension, and edema. the patient has hematuria, hypertension, and oliguria. UA shows hematuria and possibly mild proteinuria.


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First_Aid_Step2. UA shows hematuria and possibly mild proteinuria. Patients have a ↓ GFR with elevated BUN and creatinine. Complement, ANA, ANCA, and anti-GBM antibody levels should be measured to determine the underlying etiology. Renal biopsy may be useful for histologic evaluation. T AB LE 2.1 6-6. Causes of Nephritic Syndrome


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First_Aid_Step2. Immune complex Postinfectious glomerulonephritis IgA nephropathy (Berger’s disease) Classically associated with recent group A β-hemolytic streptococcal infection, but can be seen with any infection (usually 2–6 weeks prior). The most common type; associated with upper respiratory or GI infections. Commonly seen in young males; may be seen in Henoch-Schlein purpura. Oliguria, edema, hypertension, teaor cola-colored urine. Episodic gross hematuria or persistent microscopic hematuria. Low serum C3 that normalizes 6–8 weeks after presentation; ↑ASO titer; lumpy-bumpy immunoﬂ uorescence. Normal C3. Supportive. Almost all children and most adults have a complete recovery. Glucocorticoids for select patients; ACEIs in patients with proteinuria. Some 20% of cases progress to end-stage renal disease (ESRD). Pauci-immune Wegener’s granulomatosis Granulomatous inf ammation of the respiratory tract and kidney with necrotizing vasculitis. Fever, weight loss, hematuria, hearing disturbances,


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First_Aid_Step2. disease (ESRD). Pauci-immune Wegener’s granulomatosis Granulomatous inf ammation of the respiratory tract and kidney with necrotizing vasculitis. Fever, weight loss, hematuria, hearing disturbances, respiratory and sinus symptoms. Cavitary pulmonary lesions bleed and lead to hemoptysis. Presence of c-ANCA (cell-mediated immune response). Renal biopsy shows segmental necrotizing glomerulonephritis with few immunoglobulin deposits on immunof uorescence. High-dose corticosteroids and cytotoxic agents. Patients tend to have frequent relapses. Anti-GBH disease Goodpasture’s syndrome Alport’s syndrome Rapidly progressing glomerulonephritis with pulmonary hemorrhage; peak incidence is in males in their mid-20s. Hereditary glomerulonephritis; presents in boys 5–20 years of age. Hemoptysis, dyspnea, possible respiratory failure. Asymptomatic hematuria associated with nerve deafness and eye disorders. Linear anti-GBM deposits on immunof uorescence; iron def ciency anemia; hemosiderin-f lled


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First_Aid_Step2. possible respiratory failure. Asymptomatic hematuria associated with nerve deafness and eye disorders. Linear anti-GBM deposits on immunof uorescence; iron def ciency anemia; hemosiderin-f lled macrophages in sputum; pulmonary infltrates on CXR. GBM splitting on electron microscopy. Plasma exchange therapy; pulsed steroids. May progress to ESRD. Progresses to renal failure. Anti-GBM nephritis may recur after transplant.


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First_Aid_Step2. Treat hypertension, ﬂuid overload, and uremia with salt and water restriction, diuretics, and, if necessary, dialysis. In some cases, corticosteroids are useful in reducing glomerular inﬂ ammation. Defined as proteinuria (≥ 3.5 g/day), generalized edema, hypoalbuminemia, and hyperlipidemia. Approximately one-third of all cases result from systemic diseases such as DM, SLE, or amyloidosis. Causes are summarized in Table 2.16-7. TAB LE 2.1 6-7. Causes of Nephrotic Syndrome


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First_Aid_Step2. Minimal change disease The most common cause of nephrotic syndrome in children. Idiopathic etiology; 2° causes include NSAIDs and hematologic malignancies. Tendency toward infections and thrombotic events. Light microscopy appears normal; electron microscopy shows fusion of epithelial foot processes with lipid-laden renal cortices. Steroids; excellent prognosis. Focal segmental glomerulosclerosis Idiopathic, IV drug use, HIV infection, obesity. The typical patient is a young African-American male with uncontrolled hypertension. Microscopic hematuria; biopsy shows sclerosis in capillary tufts. Prednisone, cytotoxic therapy, ACEIs/ARBs to ↓ proteinuria. Membranous nephropathy The most common nephropathy in Caucasian adults. 2° causes includes solid tumor malignancies (especially in patients > 60 years of age) and immune complex disease. Associated with HBV, syphilis, malaria, and gold. “Spike-and-dome” appearance due to granular deposits of IgG and C3 at the basement membrane.


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First_Aid_Step2. patients > 60 years of age) and immune complex disease. Associated with HBV, syphilis, malaria, and gold. “Spike-and-dome” appearance due to granular deposits of IgG and C3 at the basement membrane. Prednisone and cytotoxic therapy for severe disease. Diabetic nephropathy Two characteristic forms: diffuse hyalinization and nodular glomerulosclerosis (Kimmelstiel-Wilson lesions). Generally have long-standing, poorly controlled DM with evidence of retinopathy or neuropathy. Thickened GBM; ↑mesangial matrix. Tight control of blood sugar; ACEIs for type 1 DM and ARBs for type 2 DM.


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First_Aid_Step2. TAB LE 2.1 6-7. Causes of Nephrotic Syndrome (continued)


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First_Aid_Step2. Lupus nephritis Classifed as WHO types I–VI. Both nephrotic and nephritic. The severity of renal disease often determines overall prognosis. Proteinuria or RBCs on UA may be found during evaluation of SLE patients. Mesangial proliferation; subendothelial and/or subepithelial immune complex deposition. Prednisone and cytotoxic therapy may slow disease progression. Renal amyloidosis 1° (plasma cell dyscrasia) and 2° (infectious or infammatory) are the most common. Patients may have multiple myeloma or a chronic inf ammatory disease (e.g., rheumatoid arthritis, TB). Nodular glomerulosclerosis; EM reveals amyloid f brils; apple-green birefringence with Congo red stain. Prednisone and melphalan. Bone marrow transplant may be used for multiple myeloma. Membrano-proliferative nephropathy Can also be nephritic syndrome. Type I is associated with HCV, cryoglobulinemia, SLE, and subacute bacterial endocarditis. Idiopathic form is present at 8–30 years of age. Slow progression to renal failure.


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First_Aid_Step2. be nephritic syndrome. Type I is associated with HCV, cryoglobulinemia, SLE, and subacute bacterial endocarditis. Idiopathic form is present at 8–30 years of age. Slow progression to renal failure. “Tram-track,” double-layered basement membrane. Type I has subendothelial deposits and mesangial deposits; all three types have low serum C3; type II by way of C3 nephritic factor. Corticosteroids and cytotoxic agents may help.


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First_Aid_Step2. Proteinuria, hypoalbuminemia, edema, hyperlipidemia, and hyperlipiduria in nephrotic syndrome are due to the initial ↑ in permeability of the glomerulus to protein. Presents with generalized edema and foamy urine. In severe cases, dyspnea and ascites may develop. Patients have ↑ susceptibility to infection as well as a predisposition to hypercoagulable states with an ↑ risk for venous thrombosis and pulmonary embolism. UA shows proteinuria (≥ 3.5 g/day) and lipiduria. Blood chemistry shows ↓ albumin (< 3 g/dL) and hyperlipidemia. Evaluation should include workup for 2° causes. Renal biopsy is used to definitively diagnose the underlying etiology. ■ Treat with protein and salt restriction, judicious diuretic therapy, and antihyperlipidemics. Immunosuppressant medications may be useful for certain etiologies. ACEIs ↓ proteinuria and diminish the progression of renal disease in patients with renal scarring.


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First_Aid_Step2. Immunosuppressant medications may be useful for certain etiologies. ACEIs ↓ proteinuria and diminish the progression of renal disease in patients with renal scarring. Vaccinate with 23-polyvalent pneumococcus vaccine (PPV23), as patients are at ↑ risk of Streptococcus pneumoniae infection. Renal calculi. Stones are most commonly calcium oxalate but may also be calcium phosphate, struvite, uric acid, or cystine (see Table 2.16-8 and Figure 2.16-4). Risk factors include a family history, low f uid intake, gout, medications (allopurinol, chemotherapy, loop diuretics), postcolectomy/ postileostomy, specific enzyme deficiencies, type I RTA (due to alkaline urinary pH and associated hypocitruria), and hyperparathyroidism. Most common in older males. Presents with acute onset of severe, colicky f ank pain that may radiate to the testes or vulva and is associated with nausea and vomiting.


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First_Aid_Step2. Presents with acute onset of severe, colicky f ank pain that may radiate to the testes or vulva and is associated with nausea and vomiting. Patients are unable to get comfortable and shift position frequently (as opposed to those with peritonitis, who lie still). UA may show gross or microscopic hematuria (85%) and an altered urine pH. KUB (kidney/ureter/bladder radiography) identifies radiopaque stones but will miss the 10% of stones that are radiolucent. TABLE 2.16-8. Types of Nephrolithiasis Which bacteria are associated with “staghorn calculi”? Urease-producing organisms such as Proteus.


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First_Aid_Step2. Calcium oxalate/ calcium phosphate 83% The most common causes are idiopathic hypercalciuria and 1° hyperparathyroidism. Alkaline urine. Radiopaque. Hydration, dietary sodium and protein restriction, thiazide diuretic. Avoid ↓calcium intake (can lead to hyperoxaluria and an ↑ risk of osteoporosis). Struvite (Mg-NH4 -PO4) or “triple phosphate” 9% Associated with urease-producing organisms (e.g., Proteus). Form staghorn calculi. Alkaline urine. Radiopaque. Hydration; treat UTI if present; surgical removal of staghorn stone. Uric acid 7% Associated with gout, xanthine oxidase defciency, and high purine turnover states (e.g., chemotherapy). Acidic urine (pH < 5.5). Radiolucent. Hydration; alkalinize urine with citrate, which is converted to HCO3 – in the liver; dietary purine restriction and allopurinol. Cystine 1% Due to a defect in renal transport of certain amino acids (COLA—cystine, ornithine, lysine, and arginine). Hexagonal crystals. Radiopaque. Hydration, dietary sodium restriction,


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First_Aid_Step2. Cystine 1% Due to a defect in renal transport of certain amino acids (COLA—cystine, ornithine, lysine, and arginine). Hexagonal crystals. Radiopaque. Hydration, dietary sodium restriction, alkalinization of urine, penicillamine.


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First_Aid_Step2. FIGURE 2.16-4. Nephrolithiasis. KUB shows two dense 1-cm calcifications (arrows) projecting over the midportion of the left kidney, consistent with nephrolithiasis. (Reproduced, with permission, from Chen MY, Pope TL Jr., Ott DJ. Basic Radiology, 1st ed. New York: McGraw-Hill, 2004: 243.) Noncontrast abdominal CT scans are the gold standard for the diagnosis of kidney stones. Consider a renal ultrasound to look for obstruction (ultrasound is also preferred for pregnant patients, in whom radiation from CT should be avoided). An IVP can be used to confirm the diagnosis if there is a lack of contrast filling below the stone. Hydration and analgesia are the initial treatment. Kidney stones < 5 mm in diameter can pass through the urethra; stones < 3 cm in diameter can be treated with extracorporeal shock-wave lithotripsy (ESWL), percutaneous nephrolithotomy, or retrograde ureteroscopy. Preventive measures include hydration; additional prophylaxis is dependent on stone composition.


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First_Aid_Step2. Preventive measures include hydration; additional prophylaxis is dependent on stone composition. Characterized by the presence of progressive cystic dilation of the renal tubules, as well as by cysts in the spleen, liver, and pancreas. The two major forms are as follows: ■Autosomal dominant (ADPKD): Most common. Usually asymptomatic until patients are > 30 years of age. One-half of ADPKD patients will have ESRD requiring dialysis by age 60. Associated with an ↑ risk of cerebral aneurysm, especially in patients with a family history. Autosomal recessive (ARPKD): Less common but more severe. Presents in infants and young children with renal failure, liver fibrosis, and portal hypertension; may lead to death in the first few years of life. Pain and hematuria are the most common presenting symptoms. Sharp, localized pain may result from cyst rupture, infection, or passage of renal calculi.


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First_Aid_Step2. Pain and hematuria are the most common presenting symptoms. Sharp, localized pain may result from cyst rupture, infection, or passage of renal calculi. Additional findings include hypertension, hepatic cysts, cerebral berry aneurysms, diverticulosis, and mitral valve prolapse. Patients may have large, palpable kidneys on abdominal exam. Based on ultrasound (most common) or CT scan. Multiple bilateral cysts will be present throughout the renal parenchyma, and renal enlargement will be visualized. Genetic testing by DNA linkage analysis for ADPKD1 and ADPKD2 is available. Prevent complications and ↓ the rate of progression to ESRD. Early management of UTIs is critical to prevent renal cyst infection. BP control (ACEIs, ARBs) is necessary to ↓ hypertension-induced renal damage. Dialysis and renal transplantation are used to manage patients with ESRD.


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First_Aid_Step2. Dialysis and renal transplantation are used to manage patients with ESRD. If a patient with known ADPKD develops a sudden-onset, severe headache, you must rule out subarachnoid hemorrhage from a ruptured berry aneurysm! Dilation of renal calyces. Usually occurs 2° to obstruction of the urinary tract. In pediatric patients, the obstruction is often at the ureteropelvic junction. In adults, it may be due to BPH, tumors, aortic aneurysms, or renal calculi. Can also be caused by high-output urinary ﬂow and vesicoureteral reﬂ ux. May be asymptomatic, or may present with ﬂ ank/back pain, ↓ urine output, abdominal pain, and UTIs. ■ Ultrasound or CT scan to detect dilation of the renal calyces and/or ureter. ■↑ BUN and creatinine provide evidence of 2° renal failure. Surgically correct any anatomic obstruction; use laser or sound wave lithotripsy if calculi are causing obstruction.


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First_Aid_Step2. Surgically correct any anatomic obstruction; use laser or sound wave lithotripsy if calculi are causing obstruction. Ureteral stent placement across the obstructed area of the urinary tract and/or percutaneous nephrostomy tube placement to relieve pressure may be appropriate if the urinary outﬂow tract is not sufficiently cleared of obstruction. Foley or suprapubic catheters may be required for lower urinary tract obstruction (e.g., BPH). Left untreated, hydronephrosis resulting from urinary obstruction leads to hypertension, acute or chronic renal failure, or sepsis, and has a very poor prognosis. A VCUG should be obtained in all boys presenting with their f rst UTI, girls < 3 years of age with their f rst UTI or < 5 years of age with febrile UTI, and older girls with pyelonephritis or recurrent UTIs. Bringing the testes into the scrotum does not ↓ the risk of testicular cancer.


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First_Aid_Step2. Bringing the testes into the scrotum does not ↓ the risk of testicular cancer. Retrograde projection of urine from the bladder to the ureters and kidneys. Often caused by insufficient tunneling of the ureters into submucosal bladder tissue, leading to ineffective restriction of retrograde urine ﬂow during bladder contraction. May also be due to posterior urethral valves, urethral or meatal stenosis, or a neurogenic bladder. Classified as follows: Mild refux (grades I–II): No ureteral or renal pelvic dilation. Often resolves spontaneously. Moderate to severe refux (grade III–V): Ureteral dilation with associated caliceal blunting in severe cases. Patients present with recurrent UTIs, typically in childhood. Prenatal ultrasound may identify hydronephrosis. Obtain a voiding cystourethrogram (VCUG) to detect abnormalities at ureteral insertion sites and to classify the grade of reﬂ ux. Nuclear renal scan (DMSA or MAG-3) can be used to evaluate for renal function.


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First_Aid_Step2. Nuclear renal scan (DMSA or MAG-3) can be used to evaluate for renal function. Treat infections aggressively. Treat mild reﬂux with daily prophylactic antibiotics (amoxicillin if < 2 months of age; otherwise TMP-SMX or nitrofurantoin) until reﬂ ux resolves. Surgery (ureteral reimplantation) is generally reserved for children with persistent high-grade (III to V) reﬂux or for those with breakthrough pyelonephritis while on prophylaxis. Inadequate treatment can lead to progressive renal scarring and ESRD. Failure of one or both of the testes to fully descend into the scrotum. Low birth weight is a risk factor. Bilateral cryptorchidism is associated with prematurity, oligospermia, congenital malformation syndromes (Prader-Willi, Noonan syndromes), and infertility. Associated with an ↑ risk of testicular malignancy.


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First_Aid_Step2. The testes cannot be manipulated into the scrotal sac with gentle pressure (vs. retractile testes) and may be palpated anywhere along the inguinal canal or in the abdomen. Orchiopexy by 6–12 months of age (most testes will spontaneously descend by 3 months). If discovered later, treat with orchiectomy to avoid the risk of testicular cancer. Table 2.16-9 outlines the etiologies, presentation, diagnosis, and treatment of scrotal swelling. Found in 10–25% of middle-aged and elderly men. Classified as failure to initiate (e.g., psychological, endocrinologic, neurologic), failure to fill (e.g., arteriogenic), or failure to store (e.g., veno-occlusive dysfunction). Risk factors include DM, atherosclerosis, medications (e.g., β-blockers, SSRIs, TCAs, diuretics), hypertension, heart disease, surgery or radiation for prostate cancer, and spinal cord injury. Because patients rarely volunteer this complaint, physicians should make a specific inquiry.


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First_Aid_Step2. Because patients rarely volunteer this complaint, physicians should make a specific inquiry. Ask about risk factors (diabetes, peripheral vascular disease), medication use, recent life changes, and psychological stressors. The distinction between psychological and organic ED is based on the presence of nocturnal or early-morning erections (if present, it is nonorganic) and on situation dependence (i.e., occurring with only one partner). T AB LE 2.1 6-9. Differential Diagnosis of Scrotal Swelling Painless causes Hydrocele Varicocele Remnant of the processus vaginalis. Dilation of the pampiniform venous plexus (“bag of worms”). Usually asymptomatic; transilluminates. Asymptomatic or presents with vague, aching scrotal pain. Affects the left testicle more often than the right. May disappear in the supine position. Does not transilluminate. Lab and radiologic workups are rarely indicated. Obtain an ultrasound if there is concern for inguinal hernia or testicular cancer.


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First_Aid_Step2. May disappear in the supine position. Does not transilluminate. Lab and radiologic workups are rarely indicated. Obtain an ultrasound if there is concern for inguinal hernia or testicular cancer. Ultrasound. Typically none unless hernia is present or hydrocele persists beyond 12–18 months of age (indicates patent processus vaginalis, which leads to an ↑ risk for inguinal hernia). If symptomatic or if testis makes up < 40% of total volume, may be treated surgically with a varicocelectomy or ligation, or through embolization via interventional radiology. T AB LE 2.1 6-9. Differential Diagnosis of Scrotal Swelling (continued ) Infection of the epididymis, usually from STIs, prostatitis, and/or ref ux. Twisting of the spermatic cord, leading to ischemia and possible testicular infarction. Typically affects those > 30 years of age; presents with epididymal tenderness, tender/ enlarged testicle(s), fever, scrotal thickening, erythema, and pyuria.


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First_Aid_Step2. Typically affects those > 30 years of age; presents with epididymal tenderness, tender/ enlarged testicle(s), fever, scrotal thickening, erythema, and pyuria. Pain may ↓ with scrotal elevation ( Prehn’s sign). Typically affects those < 30 years of age; presents with intense, acute-onset scrotal pain that remains the same or ↑ with scrotal elevation ( Prehn’s sign). Pain is often accompanied by nausea/vomiting and/or dizziness. Loss of cremasteric refex is also seen. UA, culture (pyuria). Culture often shows Neisseria gonorrhoeae, E. coli, or Chlamydia. Doppler ultrasound shows normal to ↑blood fow to testes. Doppler ultrasound shows ↓blood f ow to testes. (If there is a high clinical suspicion for testicular torsion, do not wait for ultrasound and proceed immediately to surgery!) Antibiotics (tetracycline, f uoroquinolones); NSAIDs; scrotal support for pain. Attempt manual detorsion.


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First_Aid_Step2. Antibiotics (tetracycline, f uoroquinolones); NSAIDs; scrotal support for pain. Attempt manual detorsion. Immediate surgery to salvage testis (the testicle is often unsalvageable after six hours of ischemia). Orchiopexy of both testes to prevent future torsion. “Point and Shoot”: The Parasympathetic nervous system mediates erection; the Sympathetic nervous system mediates ejaculation. ■ Evaluate for neurologic dysfunction (e.g., anal tone, lower extremity sensation) and for hypogonadism (e.g., small testes, loss of 2° sexual characteristics). Testosterone and gonadotropin levels may be abnormal. Check prolactin levels, as elevated prolactin can result in ↓ androgen activity. Patients with psychological ED may benefit from psychotherapy or sex therapy involving discussion and exercises with the appropriate partner.


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First_Aid_Step2. Patients with psychological ED may benefit from psychotherapy or sex therapy involving discussion and exercises with the appropriate partner. Oral sildenafl (Viagra), vardenafl (Levitra), and tadalaf l (Cialis) are phosphodiesterase-5 (PDE5) inhibitors that result in prolonged action of cGMP-mediated smooth muscle relaxation and ↑ blood ﬂow in the corpora cavernosa. Testosterone is a useful therapy for patients with hypogonadism of testicular or pituitary origin; it is discouraged for patients with normal testosterone levels. Vacuum pumps, intracavernosal prostaglandin injections, and surgical implantation of semirigid or inﬂatable penile prostheses are alternatives for patients who fail PDE5 therapy. Enlargement of the prostate that is a normal part of the aging process and is seen in > 80% of men by age 80. Most commonly presents in men > 50 years of age. BPH can result in urinary retention, recurrent UTIs, bladder and renal calculi, hydronephrosis, and kidney damage over time.


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First_Aid_Step2. Obstructive symptoms: Hesitancy, weak stream, intermittent stream, incomplete emptying, urinary retention, bladder fullness. Irritative symptoms: Nocturia, daytime frequency, urge incontinence, opening hematuria. On DRE, the prostate is uniformly enlarged with a rubbery texture. If the prostate is hard or has irregular lesions, cancer should be suspected. Conduct a DRE to screen for masses; if findings are suspicious, evaluate for prostate cancer. Obtain a UA and urine culture to rule out infection and hematuria. Measure creatinine levels to rule out obstructive uropathy and renal insufficiency. PSA testing and cystoscopy are not recommended for longitudinal BPH monitoring. Medical therapy includes α-blockers (e.g., terazosin), which relax smooth muscle in the prostate and bladder neck, as well as 5α-reductase inhibitors (e.g., finasteride), which inhibit the production of dihydrotestosterone.


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First_Aid_Step2. Transurethral resection of the prostate (TURP) or open prostatectomy is appropriate for patients with moderate to severe symptoms. The most common cancer in men and the second leading cause of cancer death in men (after lung cancer). Risk factors include advanced age and a family history. Usually asymptomatic, but may present with obstructive urinary symptoms (e.g., urinary retention, a ↓ in the force of the urine stream) as well as with lymphedema due to obstructing metastases, constitutional symptoms, and back pain due to bone metastases. DRE may reveal a palpable nodule or an area of induration. Early carcinoma is usually not detectable on exam. A tender prostate suggests prostatitis. What drugs are an absolute contraindication to sildenaf l? Nitrates (the combined effect of ↓ BP can lead to myocardial ischemia). BPH most commonly occurs in the central (periurethral) zone of the prostate and may not be detected on DRE.


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First_Aid_Step2. BPH most commonly occurs in the central (periurethral) zone of the prostate and may not be detected on DRE. The major side effect of α-blockers is orthostatic hypotension. Leading causes of cancer death in men: 1. Lung cancer 2. Prostate cancer 3. Colorectal cancer 4. Pancreatic cancer 5. Leukemia An elevated PSA may be due to BPH, prostatitis, UTI, prostatic trauma, or carcinoma. An annual DRE after age 50 is the recommended screening method for prostate cancer. Suggested by clinical findings and/or a markedly ↑PSA (> 4 ng/mL). Definitive diagnosis is made with ultrasound-guided transrectal biopsy, which typically shows adenocarcinoma. Tumors are graded by the Gleason histologic system, which sums the scores (from 1 to 5) of the two most dysplastic samples (10 is the highest grade). Look for metastases with CXR and bone scan (metastatic lesions show an osteoblastic or ↑ bone density). Fully 40% of patients present with metastatic disease at diagnosis.


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First_Aid_Step2. Look for metastases with CXR and bone scan (metastatic lesions show an osteoblastic or ↑ bone density). Fully 40% of patients present with metastatic disease at diagnosis. Treatment is controversial, as many cases of prostate cancer are slow to progress. Treatment choice is based on the aggressiveness of the tumor and the patient’s mortality risk. Watchful waiting may be the best approach for elderly patients with low-grade tumors. Radical prostatectomy and radiation therapy (e.g., brachytherapy or external beam) are associated with an ↑ risk of incontinence and/or impotence. PSA, while controversial as a screening test, is used to follow patients post-treatment to evaluate for disease recurrence. Treat metastatic disease with androgen ablation (e.g., GnRH agonists, orchiectomy, ﬂutamide) and chemotherapy.


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First_Aid_Step2. Treat metastatic disease with androgen ablation (e.g., GnRH agonists, orchiectomy, ﬂutamide) and chemotherapy. All males > 50 years of age should have an annual DRE. Screening should begin earlier in African-American males and in those with a first-degree relative with prostate cancer. Screening with PSA is common, but its utility remains controversial. The second most common urologic cancer and the most frequent malignant tumor of the urinary tract; usually a transitional cell carcinoma. Most prevalent in males during the sixth and seventh decades. Risk factors include smoking, diets rich in meat and fat, schistosomiasis, chronic treatment with cyclophosphamide, and occupational exposure to aniline dye (a benzene derivative). Gross hematuria is the most common presenting symptom. Other urinary symptoms, such as frequency, urgency, and dysuria, may also be seen, but most patients are asymptomatic in the early stages of disease. Cystoscopy with biopsy is diagnostic.


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First_Aid_Step2. Other urinary symptoms, such as frequency, urgency, and dysuria, may also be seen, but most patients are asymptomatic in the early stages of disease. Cystoscopy with biopsy is diagnostic. UA often shows hematuria (macroor microscopic); cytology may show dysplastic cells. IVP can examine the upper urinary tract as well as defects in bladder filling. ■MRI, CT, and bone scan are important tools with which to define invasion and metastases. Treatment depends on the extent of spread beyond the bladder mucosa. Carcinoma in situ: Intravesicular chemotherapy. Superf cial cancers: Complete transurethral resection or intravesicular chemotherapy with mitomycin-C or BCG (the TB vaccine). Large, high-grade recurrent lesions: Intravesicular chemotherapy. Invasive cancers without metastases: Radical cystectomy or radiotherapy for patients who are deemed poor candidates for radical cystectomy as well as for those with unresectable local disease.


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First_Aid_Step2. Invasive cancers without metastases: Radical cystectomy or radiotherapy for patients who are deemed poor candidates for radical cystectomy as well as for those with unresectable local disease. Invasive cancers with distant metastases: Chemotherapy alone. An adenocarcinoma from tubular epithelial cells (~80–90% of all malignant tumors of the kidney). Tumors can spread along the renal vein to the IVC and can metastasize to lung and bone. Risk factors include male gender, smoking, obesity, acquired cystic kidney disease in ESRD, and von Hippel– Lindau disease. Presenting signs include hematuria, f ank pain, and a palpable f ank mass. Metastatic disease can present with weight loss and malaise. Many patients have fever or other constitutional symptoms. Left-sided varicocele may seen in males (due to tumor blockage of the left gonadal vein, which empties into the left renal vein; the right gonadal vein empties directly into the IVC).


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First_Aid_Step2. Anemia is common at presentation, but polycythemia due to ↑ erythropoietin production may be seen in 5–10% of patients. Ultrasound and/or CT to characterize the renal mass (usually complex cysts or solid tumor). Surgical resection may be curative in localized disease. Response rates from radiation or chemotherapy are only 15–30%. Newer tyrosine kinase inhibitors (sorafenib, sunitinib), which ↓ tumor angiogenesis and cell proliferation, have shown promising results and have recently been approved by the FDA for the treatment of renal cell carcinoma. The classic triad of renal cell carcinoma is hematuria, f ank pain, and a palpable f ank mass, but only 5–10% present with all three components of the triad.


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First_Aid_Step2. The classic triad of renal cell carcinoma is hematuria, f ank pain, and a palpable f ank mass, but only 5–10% present with all three components of the triad. A heterogeneous group of neoplasms. Some 95% of testicular tumors derive from germ cells, and virtually all are malignant. Cryptorchidism is associated with an ↑ risk of neoplasia in both testes. Klinefelter’s syndrome is also a risk factor. Testicular cancer is the most common malignancy in males 15–34 years of age. β-hCG in men = choriocarcinoma. Patients most often present with painless enlargement of the testes. Most testicular cancers occur between ages 15 and 30, but seminomas have a peak incidence between 40 and 50 years of age. Testicular ultrasound. CXR and abdominal/pelvic CT to evaluate for metastasis. Tumor markers are useful for diagnosis and in monitoring treatment response. β-hCG is always elevated in choriocarcinoma and is elevated in 10% of seminomas.


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First_Aid_Step2. Tumor markers are useful for diagnosis and in monitoring treatment response. β-hCG is always elevated in choriocarcinoma and is elevated in 10% of seminomas. α-fetoprotein (AFP) is often elevated in nonseminomatous germ cell tumors, particularly endodermal sinus (yolk sac) tumors. It is also elevated in hepatocellular carcinoma, hepatoblastoma, and neuroblastoma. Radical orchiectomy. Seminomas are exquisitely radiosensitive and also respond to chemotherapy. Platinum-based chemotherapy is used for nonseminomatous germ cell tumors. The steps underlying the acute management of a trauma patient can be remembered with the mnemonic ABCDE. Establishing airway patency takes precedence over all other treatment, followed by providing respiratory support and treating conditions that impair respiration, followed in turn by providing circulatory support and treating conditions that impair circulation. Airway:


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First_Aid_Step2. Airway: Start with supplemental O2 by nasal cannula or face mask for conscious patients. Use a jaw-thrust maneuver to reposition the tongue in an unconscious patient. A chin-lift maneuver can be used as a last resort but should be avoided where possible, as it requires movement of the potentially unstable C-spine. An oropharyngeal or nasopharyngeal airway may facilitate bag-mask ventilation. Perform intubation in patients with apnea, significantly depressed mental status (Glasgow Coma Scale [GCS] < 8), or impending airway compromise (e.g., significant maxillofacial trauma or inhalation injury in fires). Perform a surgical airway (cricothyroidotomy) in patients who cannot be intubated or in whom there is significant maxillofacial trauma, making intubation impractical. Maintain cervical spine stabilization/immobilization in trauma patients until the spine is appropriately cleared through exam and radiographic studies. However, never allow this concern to delay airway management.


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First_Aid_Step2. Breathing: Thorough cardiac and pulmonary exams will identify the five thoracic causes of immediate death: tension pneumothorax, cardiac tamponade, open pneumothorax, massive hemothorax, and airway obstruction. If tension pneumothorax (absent breath sounds on the affected side in combination with shock and hypoxemia) is identified, immediate needle decompression is needed. This is accomplished by placing a 16to 18-gauge angiocatheter into the second intercostal space at the midclavicular line, followed by placement of a chest tube. If open pneumothorax is identified, an occlusive dressing must be applied immediately. This must be secured on three sides only to prevent the development of tension pneumothorax.


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First_Aid_Step2. If open pneumothorax is identified, an occlusive dressing must be applied immediately. This must be secured on three sides only to prevent the development of tension pneumothorax. Massive hemothorax is diagnosed through chest tube placement and is defined as > 1000 cc of immediate blood return or > 200/hour for > 2–4 hours. The treatment for massive hemothorax is volume resuscitation followed by surgery to repair the site of bleeding. The treatment for ﬂail chest is supportive, followed by surgical fixation of the chest wall. Circulation: Apply direct pressure to any actively bleeding wounds. Place a 16-gauge IV in each antecubital fossa. Isotonic ﬂuids (LR or NS) are repleted in a 3:1 ratio (ﬂuid to blood loss). Start with a ﬂuid bolus of 1–2 L in adults; then recheck vitals and continue repletion as indicated. If the patient remains tachycardic or hypotensive after the first 2 L of isotonic ﬂuid, transfusion with packed RBCs may be indicated.


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First_Aid_Step2. If the patient remains tachycardic or hypotensive after the first 2 L of isotonic ﬂuid, transfusion with packed RBCs may be indicated. To remember the Glasgow Coma Scale, think 4-eyes, Jackson-5, V6 engine. Four points can be assigned for eye response, five points for verbal response, and six points for motor response. Patients with chest trauma and shock may have cardiac tamponade. The relevant signs are JVD, hypotension, and mufﬂed heart sounds. This can be diagnosed with bedside ultrasound. If tamponade is diagnosed, an immediate pericardiocentesis is necessary. Disability/Exposure: Disability (CNS dysfunction) is assessed and quantified with the GCS. Exposure requires that the patient be completely disrobed and assessed for injury and temperature status on both the front and back of the body. Hypothermia is a common problem in trauma and can worsen bleeding; once the exam is done, the patient should be covered with warm blankets.


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First_Aid_Step2. Once the patient is stable, conduct a full examination. For unstable patients with suspected hemoperitoneum or tamponade, do a focused abdominal sonography for trauma (FAST) scan. Four spaces are checked for blood: between the right kidney and liver (Morrison’s pouch), between the left kidney and spleen (the splenorenal recess), posterior to the bladder (the pouch of Douglas), and in the pericardium. Hemoperitoneum requires immediate surgical consultation for operative management; hemopericardium requires immediate pericardiocentesis. Radiology studies should be ordered on the basis of the patient assessment. A CXR is needed for all patients with thoracic trauma, and a head CT should be ordered for all patients with loss of consciousness or depressed mental status. A C-spine CT is needed for all patients with neck pain or tenderness, neurologic findings, or depressed mental status.


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First_Aid_Step2. After urethral injury has been ruled out, place a Foley catheter if it is necessary to monitor urine output (e.g., in hemodynamically unstable patients, patients receiving ﬂuid resuscitation, or patients undergoing major surgery). Pertinent labs should be ordered based on the mechanism of injury, suspicion of intoxication or OD, and past medical history. A rough estimate of SBP can be made on the basis of palpated pulses. Carotids correspond roughly to an SBP of 60 mmHg, femorals to an SBP of 70 mmHg, and radials to an SBP of 80 mmHg. The evaluation and treatment of penetrating trauma depend on the location and extent of the injury. Intubate early. Immediate surgical exploration is mandatory for patients with shock and active ongoing hemorrhage from neck wounds. All wounds that violate the platysma are considered true penetrating neck trauma. The neck is divided into three zones, and treatment varies according to which zone is injured (see Figure 2.17-1).


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First_Aid_Step2. All wounds that violate the platysma are considered true penetrating neck trauma. The neck is divided into three zones, and treatment varies according to which zone is injured (see Figure 2.17-1). Diagnostic workup is individualized based on the location of the wound, suspected injuries, and the preference of the trauma surgeon. Appropriate tests may include angiography of the aorta and carotid/cerebral arteries, CT scan of the neck with or without CT angiography, Doppler ultrasound, contrast esophagography, esophagoscopy, or bronchoscopy. Immediately evaluate trauma patients for tension pneumothorax, cardiac tamponade, open pneumothorax, massive hemothorax, ﬂ ail chest, and airway obstruction. FIGURE 2.17-1. Zones of the neck. (Reproduced, with permission, from Way LW. Current Surgical Diagnosis & Treatment, 10th ed. Stamford, CT: Appleton & Lange, 1994: 223.)


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First_Aid_Step2. FIGURE 2.17-1. Zones of the neck. (Reproduced, with permission, from Way LW. Current Surgical Diagnosis & Treatment, 10th ed. Stamford, CT: Appleton & Lange, 1994: 223.) Unstable patients with penetrating thoracic injuries require immediate intubation followed by assessment and treatment of the life-threatening injuries described above. Empiric placement of bilateral chest tubes may be needed if the precise nature of injury is unclear. Open thoracotomy may be indicated for patients with penetrating chest trauma leading to cardiac arrest, provided that the patient arrested in the ED or shortly before arrival. Leave any impaled objects in place until the patient is taken to the OR, as such objects may tamponade further blood loss. Beware of tension pneumothorax, open pneumothorax, massive hemothorax, ﬂail chest, cardiac tamponade, aortic disruption, diaphragmatic tear, and esophageal injury. If a previously stable chest trauma patient suddenly dies, suspect air embolism.


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First_Aid_Step2. If a previously stable chest trauma patient suddenly dies, suspect air embolism. A new diastolic murmur after chest trauma suggests aortic dissection. The absence of pain does not rule out an abdominal injury. Gunshot wounds usually require immediate exploratory laparotomy, although stable patients can be managed conservatively in select cases. Stab wounds in a hemodynamically unstable patient or in a patient with peritoneal signs or evisceration require immediate exploratory laparotomy. Stab wounds in a hemodynamically stable patient warrant a CT or FAST scan followed by close inpatient observation. ■Complete neurovascular assessment is critical; check pulses, motor function, and sensory function. Arteriography and surgical management are required for patients with suspected vascular injuries. Nerve injuries generally require surgical repair.


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First_Aid_Step2. Arteriography and surgical management are required for patients with suspected vascular injuries. Nerve injuries generally require surgical repair. Early wound irrigation and tissue debridement, not antibiotic therapy, are the most important steps in the treatment of contaminated wounds. However, do administer antibiotics and tetanus prophylaxis. A rapid deceleration head injury causes coup-contrecoup injuries, in which a bleed is noted both at the site of impact and across from the point of impact. Epidural hematomas: Lenticular in shape on head CT. Bleed is from the medial meningeal artery (the higher arterial pressure is able to push the dura away from the skull, causing the lens shape on imaging). These bleeds cannot cross suture lines but can expand rapidly and cause herniation and death. Patients classically have loss of consciousness immediately after the injury and then have a “lucid interval” after which they become comatose.


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First_Aid_Step2. Subdural hematomas: Follow the curve of the skull and result from shearing of the dural bridging veins. These bleeds can cross suture lines. In a pediatric patient, a subdural hematoma coupled with retinal hemorrhages constitutes child abuse until proven otherwise. These bleeds accumulate more slowly than epidural hematomas but can still cause death. They may present acutely (immediate), subacutely (days), or chronically (weeks). The classic cause is a rapid deceleration injury (e.g., high-speed motor vehicle accidents, ejection from vehicles, and falls from heights). Since complete aortic rupture is rapidly fatal (85% die at the scene), patients with aortic disruption who are seen in the ED usually have a contained hematoma within the adventitia. Laceration is most common just proximal to the ligamentum arteriosum.


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First_Aid_Step2. Immediate CXR reveals a widened mediastinum (> 8 cm), loss of aortic knob, pleural cap, deviation of the trachea and esophagus to the right, and depression of the left main stem bronchus. CT evaluation and/or transesophageal echocardiography (TEE) prior to surgery. Aortography is the gold standard for evaluation. Basic trauma management (ABCs); emergent surgery for defect repair. ■Three or more adjacent ribs fractured at two points, causing paradoxical inward movement of the ﬂail segment with inspiration. Other signs of suspected child abuse are spiral fractures in the limbs, bucket-handle fractures, bruises, and rib fractures. Marfan’s syndrome, syphilis, and Ehlers-Danlos syndrome all predispose to a weak aortic wall. Aortic disruption is often associated with first and second rib, scapular, and sternal fractures. Kehr’s sign: Referred shoulder pain due to diaphragmatic irritation (classically on the left due to spleen rupture).


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First_Aid_Step2. Kehr’s sign: Referred shoulder pain due to diaphragmatic irritation (classically on the left due to spleen rupture). Hx/PE: Presents with crepitus and abnormal chest wall movement. Abnormal chest wall movement may not be appreciated if the patient is splinting because of pain. Dx: Primarily clinical, although CXR, O2 saturation, and blood gases may help. Tx: O2, narcotic analgesia. Respiratory support, including intubation and mechanical ventilation, may be needed to treat hypoxemia in severe cases. Surgical fixation of the chest wall is generally needed. Cx: Respiratory compromise is a complication due to underlying pulmonary contusion. The spleen and liver are the most commonly injured organs following blunt abdominal trauma. Symptoms are consistent with signs of blood loss and include hypotension, tachycardia, and peritonitis. Suspect spleen or liver injury when lower rib fractures are present.


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First_Aid_Step2. Pancreatic rupture should be suspected after a direct epigastric blow (handlebar injury). Diaphragmatic rupture may occur with blunt or penetrating trauma. It is difficult to diagnose and often missed. Kehr’s sign may be present; radio-graphs may demonstrate abdominal viscera in the thorax. The kidneys are the most commonly injured GU organ in trauma, with injuries including renal contusion, laceration, fracture, and pedicle injury. In hemodynamically stable patients, abdominal blunt trauma can be diagnosed with FAST scan (see the 2° Survey section), CT scan, and serial abdominal exams. In hemodynamically unstable patients, abdominal blunt trauma should be treated with immediate exploratory laparotomy to look for organ injury or intra-abdominal bleeding. Most commonly occur after high-speed traumas such as motor vehicle accidents or falls from heights. Require immediate attention by the orthopedist owing to their life-threatening potential.


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First_Aid_Step2. Most commonly occur after high-speed traumas such as motor vehicle accidents or falls from heights. Require immediate attention by the orthopedist owing to their life-threatening potential. May present with an unstable pelvis upon compression. Pelvic x-rays may confirm the fracture; in a stable patient, a CT scan of the pelvis will better define the extent of injury. If hypotension and shock are present, an exsanguinating hemorrhage is likely. In the field, MAST (military antishock trousers; rarely used today) can be used to maintain adequate BP and organ perfusion. Consider embolization of bleeding vessels, emergent external pelvic fixation, or, in a hemodynamically stable patient, internal fixation. Give blood early. Hemorrhage results in death in 50% of patients. Pelvic injuries can be associated with urethral injury. It is suggested by blood at the urethral meatus; a high-riding, “ballotable” prostate; or lack of a prostate.


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First_Aid_Step2. Pelvic injuries can be associated with urethral injury. It is suggested by blood at the urethral meatus; a high-riding, “ballotable” prostate; or lack of a prostate. If present, a retrograde urethrogram must be performed to rule out injury before a Foley catheter is placed. Never explore a pelvic or retroperitoneal hematoma. Follow with serial hemoglobin and hematocrit. Table 2.17-1 summarizes the basic management of cardiac arrhythmias in an acute setting. T AB LE 2.1 7 -1. Management of Cardiac Arrhythmiasa,b Updated in 2005, CPR is 30 compressions to every two breaths for all arrest victims after puberty. Unsynchronized shock with 360 J → 360-J shock → epinephrine → 360-J shock →amiodarone or lidocaine → 360-J shock → epinephrine. Vasopressin may be given in place of the frst or second dose of epinephrine. Amiodarone, lidocaine, procainamide, or sotalol may be used for stable ventricular tachycardia.


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First_Aid_Step2. Vasopressin may be given in place of the frst or second dose of epinephrine. Amiodarone, lidocaine, procainamide, or sotalol may be used for stable ventricular tachycardia. Epinephrine or vasopressin; simultaneously search for the underlying cause (see the 5 H’s and 5 T’s mnemonic) and provide empiric treatment. Give atropine for bradycardic PEA only. If unstable, perform synchronized electrical cardioversion. If stable, control rate with vagal maneuvers (Valsalva maneuver, carotid sinus massage, or cold stimulus). If resistant to maneuvers, give up to three doses of adenosine followed by other AV-nodal blocking agents (calcium channel blockers [CCBs] or β-blockers). If unstable, perform synchronized electrical cardioversion starting at 100 J. If stable, control rate with diltiazem or β-blockers and anticoagulate if duration is > 48 hours.


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First_Aid_Step2. If unstable, perform synchronized electrical cardioversion starting at 100 J. If stable, control rate with diltiazem or β-blockers and anticoagulate if duration is > 48 hours. Elective cardioversion may be performed if duration is < 48 hours; otherwise, the clinician must anticoagulate or perform TEE prior to conversion. Do not give nodal blockers if there is evidence of Wolff-Parkinson-White syndrome (δ waves) on ECG. If symptomatic, give atropine and consider dopamine, epinephrine, and glucagon. If Mobitz II or third-degree heart block is present, place transcutaneous pacemaker pads, and have atropine at the bedside. A temporary transvenous pacemaker may be required for hemodynamically unstable patients. a In all cases, disruptions of CPR should be minimized. After a shock or administration of a drug, CPR should be resumed immedi ately, and fve cycles of CPR should be given before checking for a pulse or rhythm.


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First_Aid_Step2. b Doses of electricity listed above assume a monophasic defbrillator. Maximum energy output on more modern biphasic def brilla tors is usually 150–200 J. Asystole Epinephrine and atropine. Ventricular fbrillation or pulseless ventricular tachycardia Pulseless electrical activity (PEA) Supraventricular tachycardia (SVT) Atrial f brillation/f utter Bradycardia Possible causes of PEA— The 5 H’s and 5 T’s Hypovolemia Hypoxia Hydrogen ion: Acidosis Hyper/Hypo: K+, other metabolic Hypothermia Tablets: Drug OD, ingestion Tamponade: Cardiac Tension pneumothorax Thrombosis: Coronary Thrombosis: Pulmonary Acute-onset abdominal pain has many potential etiologies and may require immediate medical or surgical intervention. Sharp, focal pain generally implies a parietal (peritoneal) etiology; dull, diffuse pain is commonly of visceral (organ) origin. Figure 2.17-2 identifies the common causes of acute abdomen.


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First_Aid_Step2. Obtain a complete history, including the elements indicated in the mnemonic OPQRST. Obtain a full gynecologic history for females (including last menstrual period, pregnancy, and any STD symptoms). If a female has abdominal pain with cervical motion tenderness, there should be a low threshold to treat for pelvic inﬂammatory disease (PID). Perforation leads to sudden onset of diffuse, severe pain, usually with abdominal rigidity on exam. Obstruction leads to acute onset of severe, radiating, colicky pain. Patients may complain of obstipation or bilious emesis. Inﬂ ammation leads to gradual onset (over 10–12 hours) of constant, illdefined pain. Associated symptoms include the following: ■Anorexia, nausea, vomiting, changes in bowel habits, hematochezia, and melena suggest GI etiologies. Rapid onset of severe,Abrupt, excruciating pain ulcer Mesenteric thrombosis, Intermittent, colicky pain,Gradual, steady pain crescendo with free intervals Acute cholecystitis, acute cholangitis,


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First_Aid_Step2. Rapid onset of severe,Abrupt, excruciating pain ulcer Mesenteric thrombosis, Intermittent, colicky pain,Gradual, steady pain crescendo with free intervals Acute cholecystitis, acute cholangitis, Small bowelAppendicitis, FIGURE 2.17-2. Acute abdomen. The location and character of pain are helpful in the differential diagnosis of the acute abdomen. (Reproduced, with permission, from Way LW. Current Surgical Diagnosis & Treatment, 10th ed. Stamford, CT: Appleton & Lange, 1994: 444.) Fever and cough suggest pneumonia. Hematuria, pyuria, and costovertebral angle tenderness point to a GU etiology. If associated with meals, consider mesenteric ischemia, PUD, biliary disease, pancreatitis, or bowel pathology. A family history of abdominal pain may indicate familial Mediterranean fever or acute intermittent porphyria.


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First_Aid_Step2. A family history of abdominal pain may indicate familial Mediterranean fever or acute intermittent porphyria. If peritoneal signs, shock, or impending shock is present, emergent exploratory laparotomy is necessary. A positive β-hCG in the setting of shock is a ruptured ectopic pregnancy until proven otherwise. Abdominal pain plus syncope or shock in an older patient is a ruptured abdominal aortic aneurysm (AAA) until proven otherwise. If the patient is stable, a complete physical exam—including a rectal exam and, in women, a pelvic exam—is mandatory. Obtain electrolytes, LFTs, amylase, lipase, urine or serum β-hCG, UA, and a CBC with differential.


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First_Aid_Step2. Obtain electrolytes, LFTs, amylase, lipase, urine or serum β-hCG, UA, and a CBC with differential. Consider a CXR for suspected perforation or pulmonary pathology. AXR may be useful for obstruction, but CT is more sensitive and specific. CT is used to diagnose appendicitis, diverticulitis, abscess, renal stones, AAA, obstruction, and other pathology. Ultrasound is the best tool for diagnosing gallstones and gynecologic pathology. Bedside ultrasound (FAST and aortic views) can diagnose hemoperitoneum and AAA in unstable patients. Hemodynamically unstable patients must have emergent surgical management. In stable patients, expectant management may include NPO status, NG tube placement, IV ﬂuids, placement of a Foley catheter (to monitor urine output and ﬂuid status), and vital sign monitoring with serial abdominal exams and serial labs.


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First_Aid_Step2. Give broad-spectrum antibiotics to all patients with perforation or signs of sepsis. Antibiotics may also be indicated for patients with infectious processes such as cholecystitis, diverticulitis, and pyelonephritis. Type and cross all unstable patients. The inciting event is obstruction of the appendiceal lumen with subsequent inﬂammation and infection. Rising intraluminal pressure leads to vascular compromise of the appendix, ischemia, necrosis, and possible perforation. Etiologies include hypertrophied lymphoid tissue (55–65%), fecalith (35%), foreign body, tumor (e.g., carcinoid tumor), and parasites. Incidence peaks in the early teens (most patients are between 10 and 30 years of age), and the male-to-female ratio is 2:1. Presents with dull periumbilical pain lasting 1–12 hours that leads to sharp RLQ pain at McBurney’s point. Also presents with nausea, vomiting, anorexia (“hamburger sign”), and low-grade fever.


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First_Aid_Step2. Presents with dull periumbilical pain lasting 1–12 hours that leads to sharp RLQ pain at McBurney’s point. Also presents with nausea, vomiting, anorexia (“hamburger sign”), and low-grade fever. Psoas, obturator, and Rovsing’s signs are insensitive tests that may be . If the patient remembers the exact moment of pain onset, think perforation. Pneumonia can present as right or left upper quadrant abdominal pain. All female patients with an acute abdomen require a pelvic exam and a pregnancy test to rule out PID, ectopic pregnancy, and ovarian torsion. McBurney’s point is located one-third of the distance from the anterior superior iliac spine to the umbilicus. “Hamburger sign”: If a patient wants to eat, consider a diagnosis other than appendicitis. Anorexia is 80% specific for appendicitis. Psoas sign: Passive extension of the hip leading to RLQ pain. Obturator sign: Passive internal rotation of the ﬂ exed hip leading to RLQ pain.


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First_Aid_Step2. Psoas sign: Passive extension of the hip leading to RLQ pain. Obturator sign: Passive internal rotation of the ﬂ exed hip leading to RLQ pain. Rovsing’s sign: Deep palpation of the LLQ leading to RLQ pain. In perforated appendix, partial pain relief is possible, but peritoneal signs (e.g., rebound, guarding, hypotension, ↑ WBC count, fever) will ultimately develop. Children, the elderly, pregnant women, and those with retrocecal appendices may have atypical presentations that may result in misdiagnosis and ↑ mortality. Diagnosed by clinical impression. Look for fever, mild leukocytosis (11,000–15,000 cells/μL) with left shift, and UA with a few RBCs and/or WBCs. If the clinical diagnosis is unequivocal, no imaging studies are necessary. Otherwise, studies include the following: KUB: Fecalith or loss of psoas shadow. Ultrasound: Enlarged, noncompressible appendix. CT scan with contrast (95–98% sensitive): Periappendiceal stranding or ﬂuid; enlarged appendix.


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First_Aid_Step2. KUB: Fecalith or loss of psoas shadow. Ultrasound: Enlarged, noncompressible appendix. CT scan with contrast (95–98% sensitive): Periappendiceal stranding or ﬂuid; enlarged appendix. The patient should be NPO and should receive IV hydration and antibiotics with anaerobic and gram-coverage. Immediate open or laparoscopic appendectomy is the definitive treatment. If appendicitis is not found, complete exploration of the abdomen is performed. Perforation: Administer antibiotics until the patient is afebrile with a normalized WBC count; the wound should be closed by delayed 1° closure. Abscess: Treat with broad-spectrum antibiotics and percutaneous drainage; an elective appendectomy should be performed 6–8 weeks later. The second leading cause of death in children. Serious burn patients should be treated in an ICU setting. Burns can be chemical, electrical, or thermal and are categorized by depth of tissue destruction:


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First_Aid_Step2. First degree: Only the epidermis is involved. The area is painful and erythematous, but blisters are not present, and capillary refill is intact. Looks like a sunburn. Second degree: The epidermis and partial thickness of the dermis are involved. The area is painful, and blisters are present. Third degree: The epidermis, the full thickness of the dermis, and potentially deeper tissues are involved. The area is painless, white, and charred. Patients may present with obvious skin wounds, but significant deep destruction may not be visible, especially with electrical burns. Conduct a thorough airway and lung exam to assess for inhalation injury. Always assume carbon monoxide poisoning in patients with inhalation injury. Consider cyanide poisoning in closed-space fires with burning carpets and textiles. Assess the ABCs. If airway compromise is impending, intubate. Be vigilant for shock, inhalation injury, and carbon monoxide poisoning. Obtain a CXR and a carboxyhemoglobin level.


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First_Aid_Step2. Assess the ABCs. If airway compromise is impending, intubate. Be vigilant for shock, inhalation injury, and carbon monoxide poisoning. Obtain a CXR and a carboxyhemoglobin level. Evaluate the percentage of body surface area (% BSA) involved. Supportive measures; tetanus, stress ulcer prophylaxis, and IV narcotic analgesia. For secondand third-degree burns, ﬂuid repletion using the Parkland formula is critical; adjust repletion on the basis of additional insensible losses to maintain at least 1 cc/kg/hr of urine output. Topical silver sulfadiazine and mafenide may be used prophylactically; however, there is no proven benefit associated with the use of PO/IV antibiotics or corticosteroids. Shock and superinfection, with the latter most likely due to Pseudomonas or gramcocci. Criteria for transfer to a burn center include the following: Full-thickness burn > 5% of BSA. Partial-thickness burn > 10% BSA.


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First_Aid_Step2. Criteria for transfer to a burn center include the following: Full-thickness burn > 5% of BSA. Partial-thickness burn > 10% BSA. Any fullor partial-thickness burn over critical areas (face, hands, feet, genitals, perineum, major joints). Circumferential burns; chemical, electrical, or lightning injury; inhalation injury. Any special psychosocial or rehabilitative care needs. Use the “rule of 9’s” to estimate % BSA in adults: Parkland formula: Fluids for the first 24 hours = 4 ×patient’s weight in kg × % BSA. Give 50% of ﬂ uids over the first eight hours and the remaining 50% over the following 16 hours. The 5 W’s of postoperative fever: Wind: Atelectasis,


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First_Aid_Step2. The 5 W’s of postoperative fever: Wind: Atelectasis, Occurs in 40% of all postoperative patients. Remember the mnemonic “Wind, Water, Wounds, Walking, and Wonder drugs.” ■↓ the risk of postoperative fever with incentive spirometry, preand postoperative antibiotics when indicated, short-term Foley catheter use, early ambulation, and DVT prophylaxis (e.g., anticoagulation, compression stockings). Fevers before postoperative day 3 are unlikely to be infectious unless Clostridium or β-hemolytic streptococci are involved. pneumonia Water: UTI Wounds: Wound infection, abscess Walking: DVT Wonder drugs: Drug ■A body temperature < 95° F (35° C) accompanied by mental status and neurologic deficits. TABLE 2.17-2. Types of Shock


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First_Aid_Step2. Hypovolemic Trauma, blood loss, dehydration with inadequate f uid repletion, third spacing, burns. ↓↓↑Replete with isotonic solution (e.g., LR or NS) and blood in a 3:1 (f uid-to-blood) ratio. Cardiogenic CHF, arrhythmia, structural heart disease (severe mitral regurgitation, VSD), Ml (> 40% of left ventricular function). ↓↑↑Identify the cause and treat if possible. Give inotropic support with pressors such as dopamine (if hypotensive) or dobutamine (if not hypotensive). Obstructive Cardiac tamponade, tension pneumothorax, massive pulmonary embolism. ↓↑↑Treat the underlying cause: pericardiocentesis, decompression of pneumothorax, thrombolysis. Bacteremia, especially gram-organisms. ↑↓↓Administer broad-spectrum antibiotics. Measure central venous pressure (CVP) and give fuid until CVP = 8. Then give pressors (dopamine or norepinephrine). Obtain cultures prior to administration of antibiotics if possible. Bee stings, medication, food allergies. ↑↓↓Give diphenhydramine. If severe,


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First_Aid_Step2. = 8. Then give pressors (dopamine or norepinephrine). Obtain cultures prior to administration of antibiotics if possible. Bee stings, medication, food allergies. ↑↓↓Give diphenhydramine. If severe, administer 1:1000 epinephrine. a PCWP = pulmonary capillary wedge pressure. b PVR = peripheral vascular resistance.


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First_Aid_Step2. Remove the patient from the cold or windy environment and remove wet clothing. In mild cases, rewarm the patient with blankets or warm water. In more severe cases, the patient may need a heating blanket, warmed oxygen, or warm IV ﬂuids. In unstable patients, invasive rewarming may be necessary (e.g., NG or bladder lavage, pleural lavage, or cardiac bypass). If the patient has frostbite, thaw the affected areas with the same methods. Patients will need narcotic analgesia for thawing. Monitor the ECG for arrhythmias such as bradycardia and slow atrial fibrillation. The stereotypic sign is the J wave (aka Osborn wave). Also monitor electrolytes and acid-base balance. Do not stop resuscitation efforts until the patient has been warmed. A body temperature > 104° F (40° C), possibly from heat stroke. Cool the patient with cold water, wet blankets, and ice. Consider a benzodiazepine to prevent convulsions. Rule out causes of fever such as infection or drug reaction.


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First_Aid_Step2. Cool the patient with cold water, wet blankets, and ice. Consider a benzodiazepine to prevent convulsions. Rule out causes of fever such as infection or drug reaction. A hypoxemic poisoning syndrome seen in patients who have been exposed to automobile exhaust, smoke inhalation, barbecues, or old appliances in poorly ventilated locations. Presents with hypoxemia, cherry-red skin (rare), confusion, and headaches. Coma or seizures occur in severe cases. Chronic low-level exposure may cause ﬂ ulike symptoms with generalized myalgias, nausea, and headaches. Ask about symptoms in others living in the same house. Suspect smoke inhalation in the presence of singed nose hairs, facial burns, hoarseness, wheezing, or carbonaceous sputum. Check an ABG and serum carboxyhemoglobin level (normal is < 5% in nonsmokers and < 10% in smokers). Check an ECG in the elderly and in patients with a history of cardiac disease.


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First_Aid_Step2. Check an ABG and serum carboxyhemoglobin level (normal is < 5% in nonsmokers and < 10% in smokers). Check an ECG in the elderly and in patients with a history of cardiac disease. Treat with 100% O2 until asymptomatic and carboxyhemoglobin falls to normal levels. Use hyperbaric O2 for pregnant patients, nonresponders, those with signs of CNS or cardiac ischemia, or those with severely ↑ carboxyhemoglobin to facilitate displacement of carbon monoxide from hemoglobin. Patients with airway burns or smoke inhalation may require early intubation, since upper airway edema can rapidly lead to complete obstruction. Table 2.17-3 outlines drug interactions and reactions that are commonly encountered in a clinical setting. Table 2.17-4 summarizes antidotes and treatments for substances commonly encountered in overdoses and intoxications. If a patient is unresponsive, it is common to empirically treat with a dose of Narcan.


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First_Aid_Step2. Malignant hyperthermia and neuroleptic malignant syndrome (NMS) should be ruled out in any suspected case of hyperthermia. Malignant hyperthermia would be seen after halothane exposure, and NMS after a neuroleptic. Both conditions are treated with dantrolene. In carbon monoxide poisoning, the patient’s oxygen saturation is usually normal. This is because carboxyhemoglobin is read by the pulse oximeter as a normal saturated hemoglobin molecule. T AB LE 2.1 7 -3. Drug Interactions and Reactions


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First_Aid_Step2. Induction of P-450 enzymes Barbiturates, phenytoin, carbamazepine, rifampin, quinidine, griseofulvin. Inhibition of P-450 enzymes Cimetidine, ketoconazole, INH, grapefruit, erythromycin, sulfonamides. Metabolism by P-450 enzymes Benzodiazepines, amide anesthetics, metoprolol, propranolol, nifedipine, phenytoin, quinidine, theophylline, warfarin, barbiturates. ↑ risk of digoxin toxicity Quinidine, cimetidine, amiodarone, CCBs. Competition for albumin-binding sites Warfarin, ASA, phenytoin. Blood dyscrasias Ibuprofen, quinidine, methyldopa, chemotherapeutic agents. Hemolysis in G6PD-defcient patients Sulfonamides, isoniazid (INH), ASA, ibuprofen, nitrofurantoin, primaquine, pyrimethamine, chloramphenicol. Gynecomastia Spironolactone, Estrogens, Digitalis, Cimetidine, chronic Alcohol use, Ketoconazole: “Some Excellent Drugs Create Awesome Knockers.” Stevens-Johnson syndrome Ethosuximide, sulfonamides. Photosensitivity Tetracycline, amiodarone, sulfonamides. Drug-induced SLE Procainamide,


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First_Aid_Step2. “Some Excellent Drugs Create Awesome Knockers.” Stevens-Johnson syndrome Ethosuximide, sulfonamides. Photosensitivity Tetracycline, amiodarone, sulfonamides. Drug-induced SLE Procainamide, hydralazine, INH, penicillamine, chlorpromazine, methyldopa, quinidine.


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First_Aid_Step2. TABLE 2.17-4. Specif c Antidotes Acetaminophen N-acetylcysteine. Acid/alkali ingestion Upper endoscopy to evaluate for stricture. Anticholinesterases, organophosphates Atropine, pralidoxime. Antimuscarinic/anticholinergic agents Physostigmine. Arsenic, mercury, gold Succimer, dimercaprol. β-blockers Glucagon. Barbiturates (phenobarbital) Urine alkalinization, dialysis, activated charcoal, supportive care. Benzodiazepines Flumazenil (can precipitate withdrawal). TABLE 2.17-4. Specifc Antidotes (continued)


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First_Aid_Step2. TABLE 2.17-4. Specifc Antidotes (continued) Black widow bite Calcium gluconate, methocarbamol. Carbon monoxide 100% O2, hyperbaric O2. Copper, arsenic, lead, gold Penicillamine. Cyanide Amyl nitrate, sodium nitrate, sodium thiosulfate. Digitalis Normalize K+ but avoid giving Ca++, Mg++, or lidocaine (for torsades), antidigitalis Fab. Heparin Protamine sulfate. INH Pyridoxine. Iron salts Deferoxamine. Lead Succimer, CaEDTA, dimercaprol. Methanol, ethylene glycol (antifreeze) EtOH, fomepizole, dialysis, calcium gluconate for ethylene glycol. Methemoglobin Methylene blue. Opioids Naloxone. Salicylates Urine alkalinization, dialysis, activated charcoal. TCAs Sodium bicarbonate for QRS prolongation; diazepam or lorazepam for seizures; cardiac monitor for arrhythmias. Theophylline Activated charcoal. Consider repeat doses. tPA, streptokinase Aminocaproic acid. Warfarin Vitamin K, FFP. Table 2.17-5 outlines the major side effects of select drugs. Management of Drug Withdrawal


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First_Aid_Step2. Table 2.17-5 outlines the major side effects of select drugs. Management of Drug Withdrawal Table 2.17-6 summarizes common drug withdrawal symptoms and treatment. Table 2.17-7 summarizes the signs and symptoms of key vitamin deficiencies. TABLE 2.17-5. Drug Side Effects


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First_Aid_Step2. ACEIs Cough, rash, proteinuria, angioedema, taste changes, teratogenic effects. Amantadine Ataxia, livedo reticularis. Aminoglycosides Ototoxicity, nephrotoxicity (acute tubular necrosis). Amiodarone Acute: AV block, hypotension, bradycardia. Chronic: pulmonary f brosis, peripheral deposition leading to bluish discoloration, arrhythmias, hypo-/hyperthyroidism, corneal deposition. Amphotericin Fever/rigors, nephrotoxicity, bone marrow suppression, anemia. Antipsychotics Sedation, acute dystonic reaction, akathisia, parkinsonism, tardive dyskinesia, NMS. Azoles (e.g., fuconazole) Inhibition of P-450 enzymes. AZT Thrombocytopenia, megaloblastic anemia. β-blockers Asthma exacerbation, masking of hypoglycemia, impotence, bradycardia, AV block, CHF. Benzodiazepines Sedation, dependence, respiratory depression. Bile acid resins Gl upset, malabsorption of vitamins and medications. CCBs Peripheral edema, constipation, cardiac depression. Carbamazepine Induction of P-450 enzymes,


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First_Aid_Step2. respiratory depression. Bile acid resins Gl upset, malabsorption of vitamins and medications. CCBs Peripheral edema, constipation, cardiac depression. Carbamazepine Induction of P-450 enzymes, agranulocytosis, aplastic anemia, liver toxicity. Chloramphenicol Gray baby syndrome, aplastic anemia. Cisplatin Nephrotoxicity, acoustic nerve damage. Clonidine Dry mouth; severe rebound headache and hypertension. Clozapine Agranulocytosis. Corticosteroids Mania, hyperglycemia (acute), immunosuppression, bone mineral loss, thinning of skin, easy bruising, myopathy, cataracts (chronic). Cyclophosphamide Myelosuppression, hemorrhagic cystitis. Digoxin Gl disturbance, yellow visual changes, arrhythmias (e.g., junctional tachycardia or SVT). Doxorubicin Cardiotoxicity (cardiomyopathy). Ethyl alcohol Renal dysfunction, CNS depression. Fluoroquinolones Cartilage damage in children; Achilles tendon rupture in adults. Furosemide Ototoxicity, hypokalemia, nephritis, gout. Gemf brozil Myositis,


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First_Aid_Step2. Renal dysfunction, CNS depression. Fluoroquinolones Cartilage damage in children; Achilles tendon rupture in adults. Furosemide Ototoxicity, hypokalemia, nephritis, gout. Gemf brozil Myositis, reversible ↑ in LFTs.


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First_Aid_Step2. TABLE 2.17-5. Drug Side Effects (continued)


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First_Aid_Step2. Halothane Hepatotoxicity, malignant hyperthermia. HCTZ Hypokalemia, hyponatremia, hyperuricemia, hyperglycemia, hypercalcemia. HMG-CoA reductase inhibitors Myositis, reversible ↑ in LFTs. Hydralazine Drug-induced SLE. Hydroxychloroquine Retinopathy. INH Peripheral neuropathy (prevent with pyridoxine/vitamin B6), hepatotoxicity, inhibition of P-450 enzymes, seizures with overdose, hemolysis in G6PD def ciency. MAOIs Hypertensive tyramine reaction, serotonin syndrome (with meperidine). Methanol Blindness. Methotrexate Hepatic fbrosis, pneumonitis, anemia. Methyldopa Coombs’ test, drug-induced SLE. Metronidazole Disulfram reaction, vestibular dysfunction, metallic taste. Niacin Cutaneous f ushing. Nitroglycerin Hypotension, tachycardia, headache, tolerance. Penicillamine Drug-induced SLE. Penicillin/β-lactams Hypersensitivity reactions. Phenytoin Nystagmus, diplopia, ataxia, arrhythmia (in toxic doses), gingival hyperplasia, hirsutism, teratogenic effects. Prazosin First-dose


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First_Aid_Step2. SLE. Penicillin/β-lactams Hypersensitivity reactions. Phenytoin Nystagmus, diplopia, ataxia, arrhythmia (in toxic doses), gingival hyperplasia, hirsutism, teratogenic effects. Prazosin First-dose hypotension. Procainamide Drug-induced SLE. Propylthiouracil Agranulocytosis, aplastic anemia. Quinidine Cinchonism (headache, tinnitus), thrombocytopenia, arrhythmias (e.g., torsades de pointes). Reserpine Depression. Rifampin Induction of P-450 enzymes; orange-red body secretions. Salicylates Fever; hyperventilation with respiratory alkalosis and metabolic acidosis; dehydration, diaphoresis, hemorrhagic gastritis. SSRIs Anxiety, sexual dysfunction, serotonin syndrome if taken with MAOIs.


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First_Aid_Step2. TABLE 2.17-5. Drug Side Effects (continued) Succinylcholine Malignant hyperthermia, hyperkalemia. TCAs Sedation, coma, anticholinergic effects, seizures and arrhythmias. Tetracyclines Tooth discoloration, photosensitivity, Fanconi’s syndrome, Gl distress. Trimethoprim Megaloblastic anemia, leukopenia, granulocytopenia. Valproic acid Teratogenicity leads to neural tube defects; rare fatal hepatotoxicity. Vancomycin Nephrotoxicity, ototoxicity, “red man syndrome” (histamine release; not an allergy). Vinblastine Severe myelosuppression. Vincristine Peripheral neuropathy, paralytic ileus. T AB LE 2.1 7 -6. Symptoms and Treatment of Drug Withdrawal


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First_Aid_Step2. Alcohol Tremor (6–12 hours). Tachycardia, hypertension, agitation, seizures (within 48 hours). Hallucinations, DTs—severe autonomic instability leading to tachycardia, hypertension, delirium, and possibly death (within 2–7 days). Mortality is 15–20%. Benzodiazepines (can require massive doses); haloperidol for hallucinations; thiamine, folate, and multivitamin replacement (do not affect withdrawal, but most alcoholics are def cient). Barbiturates Anxiety, seizures, delirium, tremor; cardiac and respiratory depression. Benzodiazepines. Benzodiazepines Rebound anxiety, seizures, tremor, insomnia. Benzodiazepines. Monitor for DTs. Cocaine/ amphetamines Depression, hyperphagia, hypersomnolence. Supportive treatment. Avoid pure β-blockers (may lead to unopposed α activity, causing hypertension). Opioids Anxiety, insomnia, fulike symptoms, piloerection, fever, rhinorrhea, lacrimation, yawning, nausea, stomach cramps, diarrhea, mydriasis. Antiemetics, muscle relaxers, and NSAIDs for mild


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First_Aid_Step2. Opioids Anxiety, insomnia, fulike symptoms, piloerection, fever, rhinorrhea, lacrimation, yawning, nausea, stomach cramps, diarrhea, mydriasis. Antiemetics, muscle relaxers, and NSAIDs for mild symptoms; clonidine, buprenorphine, or methadone for moderate to severe symptoms.


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First_Aid_Step2. TABLE 2.17-7. Vitamin Functions and Def ciencies


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First_Aid_Step2. Vitamin A Night blindness, dry skin. Vitamin B1 (thiamine) Beriberi (polyneuritis, dilated cardiomyopathy, high-output CHF, edema), Wernicke-Korsakoff syndrome. Vitamin B2 (ribofavin) Angular stomatitis, cheilosis, corneal vascularization. Vitamin B3 (niacin) Pellagra (diarrhea, dermatitis, dementia). Vitamin B5 (pantothenate) Dermatitis, enteritis, alopecia, adrenal insuff ciency. Vitamin B6 (pyridoxine) Convulsions, hyperirritability; required during administration of INH. Vitamin B12 (cobalamin) Macrocytic, megaloblastic anemia; neurologic symptoms (e.g., optic neuropathy, subacute combined degeneration, paresthesias); glossitis. Vitamin C Scurvy (e.g., swollen gums, bruising, anemia, poor wound healing). Vitamin D Rickets in children (bending bones), osteomalacia in adults (soft bones), hypocalcemic tetany. Vitamin E ↑ fragility of RBCs. Vitamin K Neonatal hemorrhage; ↑ PT and aPTT, normal BT. Biotin Dermatitis, enteritis. Can be caused by ingestion of raw eggs or antibiotic use.


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First_Aid_Step2. hypocalcemic tetany. Vitamin E ↑ fragility of RBCs. Vitamin K Neonatal hemorrhage; ↑ PT and aPTT, normal BT. Biotin Dermatitis, enteritis. Can be caused by ingestion of raw eggs or antibiotic use. Folic acid The most common vitamin defciency in the United States. Sprue; macrocytic, megaloblastic anemia without neurologic symptoms. Magnesium Weakness, muscle cramps, exacerbation of hypocalcemic tetany, CNS hyperirritability leading to tremors, choreoathetoid movement. Selenium Keshan disease (cardiomyopathy).


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First_Aid_Step2. Classic ECG finding in atrial ﬂutter. Definition of unstable angina. Antihypertensive for a diabetic patient with proteinuria. Beck’s triad for cardiac tamponade. Drugs that slow AV node transmission. Hypercholesterolemia treatment that leads to ﬂ ushing and pruritus. Murmur—hypertrophic obstructive cardiomyopathy (HOCM). Murmur—aortic insufficiency. Murmur—aortic stenosis. Murmur—mitral regurgitation. Murmur—mitral stenosis. Treatment for atrial fibrillation and atrial ﬂutter. Treatment for ventricular fibrillation. Autoimmune complication occurring 2–4 weeks post-MI. IV drug use with JVD and holosystolic murmur at the left sternal border. Treatment? Diagnostic test for hypertrophic cardiomyopathy. A fall in systolic BP of > 10 mmHg with inspiration. Classic ECG findings in pericarditis. Definition of hypertension. Eight surgically correctable causes of hypertension.


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First_Aid_Step2. A fall in systolic BP of > 10 mmHg with inspiration. Classic ECG findings in pericarditis. Definition of hypertension. Eight surgically correctable causes of hypertension. “Sawtooth” P waves. Angina is new, is worsening, or occurs at rest. ACEI. Hypotension, distant heart sounds, and JVD. β-blockers, digoxin, calcium channel blockers. Niacin. Systolic ejection murmur heard along the lateral sternal border that ↑ with Valsalva maneuver and standing. Diastolic, decrescendo, high-pitched, blowing murmur that is best heard sitting up; ↑ with ↓ preload (handgrip maneuver). Systolic crescendo/decrescendo murmur that radiates to the neck; ↑ with ↑ preload (Valsalva maneuver). Holosystolic murmur that radiates to the axillae or carotids. Diastolic, midto late, low-pitched murmur. If unstable, cardiovert. If stable or chronic, rate control with calcium channel blockers or β-blockers.


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First_Aid_Step2. Diastolic, midto late, low-pitched murmur. If unstable, cardiovert. If stable or chronic, rate control with calcium channel blockers or β-blockers. Immediate cardioversion. Dressler’s syndrome: fever, pericarditis, ↑ ESR. Treat existing heart failure and replace the tricuspid valve. Echocardiogram (showing thickened left ventricular wall and outﬂ ow obstruction). Pulsus paradoxus (seen in cardiac tamponade). Low-voltage, diffuse ST-segment elevation. BP > 140/90 on three separate occasions two weeks apart. Renal artery stenosis, coarctation of the aorta, pheochromocytoma, Conn’s syndrome, Cushing’s syndrome, unilateral renal parenchymal disease, hyperthyroidism, hyperparathyroidism. Evaluation of a pulsatile abdominal mass and bruit. Indications for surgical repair of abdominal aortic aneurysm. Treatment for acute coronary syndrome. What is metabolic syndrome? Appropriate diagnostic test? A 50-year-old man with angina can exercise to 85% of maximum predicted heart rate.


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First_Aid_Step2. What is metabolic syndrome? Appropriate diagnostic test? A 50-year-old man with angina can exercise to 85% of maximum predicted heart rate. A 65-year-old woman with left bundle branch block and severe osteoarthritis has unstable angina. Target LDL in a patient with diabetes. Signs of active ischemia during stress testing. ECG findings suggesting MI. Coronary territories in MI. A young patient has angina at rest with ST-segment elevation. Cardiac enzymes are normal. Common symptoms associated with silent Mls. The diagnostic test for pulmonary embolism. An agent that reverses the effects of heparin. The coagulation parameter affected by warfarin. A young patient with a family history of sudden death collapses and dies while exercising. Endocarditis prophylaxis regimens. The 6 P’s of ischemia due to peripheral vascular disease. Virchow’s triad. The most common cause of hypertension in young women. The most common cause of hypertension in young men.


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First_Aid_Step2. The 6 P’s of ischemia due to peripheral vascular disease. Virchow’s triad. The most common cause of hypertension in young women. The most common cause of hypertension in young men. Abdominal ultrasound and CT. > 5.5 cm, rapidly enlarging, symptomatic, or ruptured. Morphine, O2, sublingual nitroglycerin, ASA, IV β-blockers, heparin. Abdominal obesity, high triglycerides, low HDL, hypertension, insulin resistance, prothrombotic or proinﬂ ammatory states. Exercise stress treadmill with ECG. Pharmacologic stress test (e.g., dobutamine echo). < 70. Angina, ST-segment changes on ECG, or ↓ BP. ST-segment elevation (depression means ischemia), ﬂattened T waves, and Q waves. Anterior wall (LAD/diagonal), inferior (PDA), posterior (left circumﬂex/oblique, RCA/marginal), septum (LAD/diagonal). Prinzmetal’s angina. CHF, shock, and altered mental status. V/Q scan. Protamine. PT. Hypertrophic cardiomyopathy.


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First_Aid_Step2. CHF, shock, and altered mental status. V/Q scan. Protamine. PT. Hypertrophic cardiomyopathy. and gentamicin before and amoxicillin after. Pain, pallor, pulselessness, paralysis, paresthesia, poikilothermia. Stasis, hypercoagulability, endothelial damage. OCPs. Excessive EtOH. “Stuck-on” appearance. Red plaques with silvery-white scales and sharp margins. The most common type of skin cancer; the lesion is a pearly-colored papule with a translucent surface and telangiectasias. Honey-crusted lesions. A febrile patient with a history of diabetes presents with a red, swollen, painful lower extremity. Nikolsky’s sign. Nikolsky’s sign. A 55-year-old obese patient presents with dirty, velvety patches on the back of the neck. Dermatomal distribution. Flat-topped papules. Iris-like target lesions. A lesion characteristically occurring in a linear pattern in areas where skin comes into contact with clothing or jewelry.


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First_Aid_Step2. Presents with a herald patch, Christmas-tree pattern. A 16-year-old presents with an annular patch of alopecia with broken-off, stubby hairs. Pinkish, scaling, ﬂat lesions on the chest and back; KOH prep has a “spaghetti-and-meatballs” appearance. Four characteristics of a nevus suggestive of melanoma. A premalignant lesion from sun exposure that can lead to squamous cell carcinoma. “Dewdrops on a rose petal.” “Cradle cap.” Associated with Propionibacterium acnes and changes in androgen levels. Seborrheic keratosis. Psoriasis. Basal cell carcinoma. Impetigo. Cellulitis. Pemphigus vulgaris. Bullous pemphigoid. Acanthosis nigricans. Check fasting blood glucose to rule out diabetes. Varicella zoster. Lichen planus. Erythema multiforme. Contact dermatitis. Pityriasis rosea. Alopecia areata (an autoimmune process). Pityriasis versicolor. Asymmetry, border irregularity, color variation, and large diameter. Actinic keratosis.


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First_Aid_Step2. Pityriasis rosea. Alopecia areata (an autoimmune process). Pityriasis versicolor. Asymmetry, border irregularity, color variation, and large diameter. Actinic keratosis. Lesions of 1° varicella. Seborrheic dermatitis. Treat with antifungals. Acne vulgaris. A painful, recurrent vesicular eruption of mucocutaneous surfaces. Inﬂammation and epithelial thinning of the anogenital area, predominantly in postmenopausal women. Exophytic nodules on the skin with varying degrees of scaling or ulceration; the second most common type of skin cancer. Herpes simplex. Lichen sclerosus. Squamous cell carcinoma. Bias introduced into a study when a clinician is aware of the patient’s treatment type. Bias introduced when screening detects a disease earlier and thus lengthens the time from diagnosis to death.


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First_Aid_Step2. Bias introduced into a study when a clinician is aware of the patient’s treatment type. Bias introduced when screening detects a disease earlier and thus lengthens the time from diagnosis to death. If you want to know if geographical location affects infant mortality rate but most variation in infant mortality is predicted by socioeconomic status, then socioeconomic status is a _____. The number of true positives divided by the number of patients with the disease is _____. Sensitive tests have few false negatives and are used to rule _____ a disease. PPD reactivity is used as a screening test because most people with TB (except those who are anergic) will have a PPD. Highly sensitive or specific? Chronic diseases such as SLE—higher prevalence or incidence? Epidemics such as inﬂuenza—higher prevalence or incidence? Cross-sectional survey—incidence or prevalence? Cohort study—incidence or prevalence? Case-control study—incidence or prevalence?


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First_Aid_Step2. Epidemics such as inﬂuenza—higher prevalence or incidence? Cross-sectional survey—incidence or prevalence? Cohort study—incidence or prevalence? Case-control study—incidence or prevalence? Describe a test that consistently gives identical results, but the results are wrong. Difference between a cohort and a case-control study. Observational bias. Lead-time bias. Confounding variable. Sensitivity. Out. Highly sensitive for TB. Higher prevalence. Higher incidence. Prevalence. Incidence and prevalence. Neither. High reliability, low validity. Cohort studies can be used to calculate relative risk (RR), incidence, and/or odds ratio (OR). Case-control studies can be used to calculate an OR. Attributable risk? Relative risk? Odds ratio? Number needed to treat? In which patients do you initiate colorectal cancer screening early?


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First_Aid_Step2. Attributable risk? Relative risk? Odds ratio? Number needed to treat? In which patients do you initiate colorectal cancer screening early? The most common cancer in men and the most common cause of death from cancer in men. The percentage of cases within one SD of the mean? Two SDs? Three SDs? Birth rate? Fertility rate? Mortality rate? Neonatal mortality rate? Postnatal mortality rate? Infant mortality rate? Fetal mortality rate? Perinatal mortality rate? Maternal mortality rate? The incidence rate (IR) of a disease in exposed – the IR of a disease in unexposed. The IR of a disease in a population exposed to a particular factor ÷ the IR of those not exposed. The likelihood of a disease among individuals exposed to a risk factor compared to those who have not been exposed. 1 ÷ (rate in untreated group – rate in treated group).


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First_Aid_Step2. The likelihood of a disease among individuals exposed to a risk factor compared to those who have not been exposed. 1 ÷ (rate in untreated group – rate in treated group). Patients with IBD; those with familial adenomatous polyposis (FAP)/hereditary nonpolyposis colorectal cancer (HNPCC); and those who have first-degree relatives with adenomatous polyps (< 60 years of age) or colorectal cancer. Prostate cancer is the most common cancer in men, but lung cancer causes more deaths. 68%, 95.4%, 99.7%. Number of live births per 1000 population in one year. Number of live births per 1000 females (15–44 years of age) in one year. Number of deaths per 1000 population in one year. Number of deaths from birth to 28 days per 1000 live births in one year. Number of deaths from 28 days to one year per 1000 live births in one year. Number of deaths from birth to one year of age per 1000 live births (neonatal + postnatal mortality) in one year.


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First_Aid_Step2. Number of deaths from 28 days to one year per 1000 live births in one year. Number of deaths from birth to one year of age per 1000 live births (neonatal + postnatal mortality) in one year. Number of deaths from 20 weeks’ gestation to birth per 1000 total births in one year. Number of deaths from 20 weeks’ gestation to one month of life per 1000 total births in one year. Number of deaths during pregnancy to 90 days postpartum per 100,000 live births in one year. True or false: Once patients sign a statement giving consent, they must continue treatment. A 15-year-old pregnant girl requires hospitalization for preeclampsia. Is parental consent required? A doctor refers a patient for an MRI at a facility he/she owns. Involuntary psychiatric hospitalization can be undertaken for which three reasons? True or false: Withdrawing a nonbeneficial treatment is ethically similar to withholding a nonindicated one.


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First_Aid_Step2. Involuntary psychiatric hospitalization can be undertaken for which three reasons? True or false: Withdrawing a nonbeneficial treatment is ethically similar to withholding a nonindicated one. When can a physician refuse to continue treating a patient on the grounds of futility? An eight-year-old child is in a serious accident. She requires emergent transfusion, but her parents are not present. Conditions in which confidentiality must be overridden. Involuntary commitment or isolation for medical treatment may be undertaken for what reason? A 10-year-old child presents in status epilepticus, but her parents refuse treatment on religious grounds. A son asks that his mother not be told about her recently discovered cancer. False. Patients may change their minds at any time. Exceptions to the requirement of informed consent include emergency situations and patients without decision-making capacity.


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First_Aid_Step2. False. Patients may change their minds at any time. Exceptions to the requirement of informed consent include emergency situations and patients without decision-making capacity. No. Parental consent is not necessary for the medical treatment of pregnant minors. Conﬂict of interest. The patient is a danger to self, a danger to others, or gravely disabled (unable to provide for basic needs). True. When there is no rationale for treatment, maximal intervention is failing, a given intervention has already failed, and treatment will not achieve the goals of care. Treat immediately. Consent is implied in emergency situations. Real threat of harm to third parties; suicidal intentions; certain contagious diseases; elder and child abuse. When treatment noncompliance represents a serious danger to public health (e.g., active TB). Treat because the disease represents an immediate threat to the child’s life. Then seek a court order.


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First_Aid_Step2. When treatment noncompliance represents a serious danger to public health (e.g., active TB). Treat because the disease represents an immediate threat to the child’s life. Then seek a court order. A physician can withhold information from the patient only in the rare case of therapeutic privilege or if the patient requests not to be told. A patient’s family cannot require the physician to withhold information from the patient. Diagnostic modality used when ultrasound is equivocal for cholecystitis. Risk factors for cholelithiasis. Inspiratory arrest during palpation of the RUQ. The most common cause of SBO in patients with no history of abdominal surgery. The most common cause of SBO in patients with a history of abdominal surgery. Identify key organisms causing diarrhea: A 25-year-old Jewish man presents with pain and watery diarrhea after meals. Exam shows fistulas between the bowel and skin and nodular lesions on his tibias.


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First_Aid_Step2. A 25-year-old Jewish man presents with pain and watery diarrhea after meals. Exam shows fistulas between the bowel and skin and nodular lesions on his tibias. Inﬂammatory disease of the colon with ↑ risk of colon cancer. Extraintestinal manifestations of IBD. Medical treatment for IBD. Difference between Mallory-Weiss and Boerhaave tears. Charcot’s triad. Reynolds’ pentad. Medical treatment for hepatic encephalopathy. HIDA scan. Fat, female, fertile, forty, ﬂ atulent. Murphy’s sign, seen in acute cholecystitis. Hernia. Adhesions. S. aureus E. coli O157:H7 Bacillus cereus Salmonella Vibrio, HAV Isospora, Cryptosporidium, Mycobacterium avium complex Crohn’s disease. Ulcerative colitis (greater risk than Crohn’s). Uveitis, ankylosing spondylitis, pyoderma gangrenosum, erythema nodosum, 1° sclerosing cholangitis. 5-ASA agents and steroids during acute exacerbations. Mallory-Weiss—superficial tear in the esophageal mucosa; Boerhaave—full-thickness esophageal rupture.


First_Aid_Step2

First_Aid_Step2. 5-ASA agents and steroids during acute exacerbations. Mallory-Weiss—superficial tear in the esophageal mucosa; Boerhaave—full-thickness esophageal rupture. RUQ pain, jaundice, and fever/chills in the setting of ascending cholangitis. Charcot’s triad plus shock and mental status changes, with suppurative ascending cholangitis. ↓ protein intake, lactulose, rifaximin. First step in the management of a patient with an acute GI bleed. A four-year-old child presents with oliguria, petechiae, and jaundice following an illness with bloody diarrhea. Most likely diagnosis and cause? Post-HBV exposure treatment. Classic causes of drug-induced hepatitis. A 40-year-old obese woman with elevated alkaline phosphatase, elevated bilirubin, pruritus, dark urine, and clay-colored stools. Hernia with highest risk of incarceration—indirect, direct, or femoral?


First_Aid_Step2

First_Aid_Step2. Hernia with highest risk of incarceration—indirect, direct, or femoral? A 50-year-old man with a history of alcohol abuse presents with boring epigastric pain that radiates to the back and is relieved by sitting forward. Management? Establish the ABCs. Hemolytic-uremic syndrome (HUS) due to E. coli O157: H7. HBV immunoglobulin. TB medications (INH, rifampin, pyrazinamide), acetaminophen, and tetracycline. Biliary tract obstruction. Femoral hernia. Confirm the diagnosis of acute pancreatitis with elevated amylase and lipase. Make the patient NPO and give IV ﬂ uids, O2, analgesia, and “tincture of time.” Four causes of microcytic anemia. An elderly man with hypochromic, microcytic anemia is asymptomatic. Diagnostic tests? Precipitants of hemolytic crisis in patients with G6PD deficiency.