Evaluate the extent (severity) of the bleeding and assess hemodynamic stability.
Locate the site of the bleeding:• Upper GI bleeding (above the ligament of Treitz): PUD (40%-79%), gastritis/duodenitis (5%-30%), esophageal or gastric varices (6%-21%), Mallory-Weiss tears (3%-15%), tumors (2%-3%), AV (<1%) and aortoenteric fistulas (<1%)
• Lower GI bleeding (below the ligament of Treitz): Acute massive lower GI bleeding causes are diverticular disease (17%-40%), angiodysplasia (2%-30% of colonic bleeding, 70%-80% of small bowel bleeding), neoplasm (11%-14%), IBD (9%-21%), ischemic colitis (5%), solitary rectal ulcer (2%-5%), NSAID-induced colonic ulceration (1%), acute infectious colitis (1%), pseudomembranous colitis (1%), postpolypectomy bleeding (2%-5%), radiation colitis (2%-5%), hemorrhoids (1%), and anal fissures (1%).
Hx
Meds (ASA, steroids, “blood thinners,” NSAIDs)
Prior GI or vascular surgery
H/o GI dx or bleeding
Smoking
Alcohol intake (gastritis, esophageal varices)
Sx of PUD
Associated diseases (CAD, diabetes, HTN, hematologic disorders, renal failure)
Protracted retching and vomiting (consider gastric or gastroesophageal tear [Mallory-Weiss syndrome])
Weight loss, anorexia (consider carcinoma)
Color and character of stool (i.e., hematochezia or melena, constipation or diarrhea)
Presence or absence of hematemesisPE
VS: tachycardia, hypotension, postural changes (orthostatic hypotension). A pulse ↑ >20 bpm or a postural ↑ in systolic BP >10 to 15 mm Hg indicates blood loss >1 L.
Pts taking β-adrenergic blockers may not demonstrate significant tachycardia w/volume depletion.
Cardiorespiratory exam: murmurs (↑ incidence of angiodysplasia in pts w/AS), pulmonary rales, JVD to determine rapidity of volume replacement
Abd exam:• Observe for masses, tenderness, distention, ascites.
• Auscultate for bowel sounds or abd bruits.
• Look for evidence of liver disease (hepatomegaly, splenomegaly, abnl vascular patterns, gynecomastia, spider angiomas, palmar erythema, testicular atrophy).
DRE: Check for masses, strictures, hemorrhoids; test stool for occult blood and inspect it for abnormalities (tarry, blood streaked, bright red, mahogany color).
Skin: Check for jaundice (liver disease), ecchymoses (coagulation abnormality), cutaneous telangiectasia (Rendu-Osler-Weber disease), buccal pigmentation (Peutz-Jeghers syndrome), and other mucocutaneous changes (Ehlers-Danlos syndrome).
Look for evidence of metastatic disease (cachexia, firm nodular liver).
If the pt is not experiencing hematemesis and endoscopy is not immediately available, an NG tube may be placed for gastric lavage while awaiting endoscopy to determine whether the bleeding is emanating from the UGI tract (presence of bright red blood clots or coffee-ground–like guaiac (+) aspirate); however, the sensitivity and specificity of this process are limited. A (−) aspirate does not r/o upper GI bleeding because it could have subsided or the pt could be bleeding from the duodenal bulb w/o reflux into the stomach. Lavage w/500 mL of NS. Failure to clear blood w/gastric lavage indicates persistent bleeding and the need for more urgent endoscopy.Initial Management
Stabilize the pt: Insert two large-bore (18-gauge) IV catheters and administer lactated Ringer’s solution or NS; the rate of volume replacement is based on the estimated blood loss, clinical condition, and h/o CVD, including CHF.
Type and crossmatch for 2 to 8 U of PRBCs, depending on the estimated blood loss, and transfuse as necessary. Aim for Hct >30 for elderly pts w/multiple comorbid conditions and ≥20 for young, healthy individuals.
Initial labs:• Hgb/Hct
• Initial value should be considered erroneous until serum volume is replaced by crystalloid fluid.
• After bleeding ceases, the Hct may continue to ↓ for up to 6 hr, and full equilibration may require 24 hr. Follow the Hgb/Hct q6-8 hr while active bleeding is present.
• The Hct generally ↓ by 2 to 3 points and the Hgb falls by 1 point for every 500 mL of blood lost.
• BUN: In the absence of renal disease, the BUN level may help determine the severity of the bleeding; a simultaneous Cr level may also be of value because the disparity in the BUN/Cr ratio will reveal the extent of the bleeding more accurately; BUN/Cr >36 is suggestive of UGI bleeding. BUN levels can be confusing if the bleeding is insidious and may mark prerenal azotemia secondary to the bleeding.
• PT, APTT, and Plt count should be calculated to exclude bleeding disorders; other useful initial labs are LFTs, serum electrolytes, and glucose.
ECG: R/o myocardial ischemia secondary to severe anemia in patients with risk factors.Endoscopic EzZvaluation
EGD is indicated when blood or guaiac (+) coffee ground–like material is obtained from the NG aspirate or if lower endoscopic findings are (−). It should be performed urgently in hemodynamically unstable pts or those found to still be actively bleeding by NG lavage or in those requiring blood transfusion. Otherwise, it should ideally be performed within 24 hr of the hospital admission. In addition, if a therapeutic procedure (e.g., bipolar heater probe, laser cauterization, injection scleroRx, or band ligation) is considered, endoscopy should be done on an emergency basis.
Colonoscopy should be performed initially if lower GI bleeding is suspected, generally within 24 hr of hospital admission after adequate bowel preparation.Imaging
Arteriography can identify briskly bleeding sources. Overall diagnostic sensitivity of arteriography is 41%. Mesenteric arteriography is useful to identify bleeding from AV malformations.
Radionuclide scans may be used before angiography to determine which pts are bleeding sufficiently to make (+) angiographic result more likely. Bleeding at rates as low as 0.1 mL/min can be detected by radionuclide scans. A (+) “immediate blush” is a good indication for urgent angiography, whereas a (−) “delayed blush” is an indication for observation and elective colonoscopy.
Technetium-99m (99mTc) pertechnetate scan (Meckel scan) selectively tags acid-secreting cells (gastric mucosa); it is used most often for unexplained bleeding in infants and young adults.
99mTc-sulfur colloid scan is very sensitive in detecting lesions w/low bleeding rates; its major drawbacks are as follows:• Short half-life (difficulty in detecting intermittent bleeding)
• Affinity of the colloid for liver and spleen (colonic bleeding may be missed if it originates in a region superimposed on areas of liver or spleen uptake)
99mTc-labeled RBC scan: Its major advantage over the sulfur colloid scan is its long duration; it is useful for intermittent bleeding because the pt can be monitored for GI bleeding for 24 to 48 hr. Its disadvantage is that it has a high false-localization rate.
Selective angiography:• On occasion, this is the first test ordered in actively bleeding pts, but in most situations, it is reserved for massive, ongoing bleeding, especially when endoscopy is not feasible or when endoscopic evaluation is unrevealing w/recurrent or persistent blood loss.
• Angiography may also be therapeutic because vasoconstrictors, autologous clots, or Gelfoam emboli can be administered intra-arterially at the time of angiography to occlude the bleeding vessel.
• Major drawbacks are the high rate of bleeding (>0.5 mL/min) necessary for dx and the risk of allergic reaction to the contrast dye.
• Advantages include the fact that no bowel preparation is required and anatomic localization is accurate.
• Enhanced helical CT scanning w/IV contrast material is used in selected cases.
Treatment
Correct bleeding abnormalities by administering FFP or vitamin K if the pt has a coagulopathy and Plt if the pt is severely thrombocytopenic.
IV PPIs in cases of probable peptic ulcer or gastritis. After endoscopic Rx of bleeding peptic ulcers, IV PPIs ↓ the risk of recurrent bleeding ↑ pH, ↑ platelet function.
Octreotide: IV bolus of 50 to 100 μg followed by IV infusion of 25 to 50 μg/hr is useful for acute variceal bleeding. Another useful agent is terlipressin.
Endoscopy:• ScleroRx or endoscopic variceal ligation is used for bleeding varices.
• Injection Rx (e.g., epinephrine, saline), bipolar electrocoagulation, and heater-probe Rx are equally effective modalities in the Rx of bleeding peptic ulcer.
Balloon tamponade is indicated for severe bleeding from esophageal varices if octreotide or other endoscopic Rx modalities are ineffective.
Radiologic modalities include localized infusion of vasopressin, autologous clots, or foreign coagulating substances (e.g., Gelfoam) in the bleeding vessel during or after arteriography.
Surgery is indicated at the onset of dx of aortoduodenal fistula, but it is not suggested as the initial Rx in cases of other causes of GI bleeding until a definitive dx is made and other noninvasive modalities are tried. Surgical approach may be necessary in the following situations:• Rebleeding in a hospitalized pt
• Bleeding episode that requires transfusion of >4 U of PRBCs in 24 hr or >10 U of PRBCs in total
• Endoscopic visualization of a “naked” vessel in a peptic ulcer unresponsive to injection or coagulation Rx
B. Disorders of the Esophagus
1. Dysphagia
a. Oropharyngeal Dysphagia
Inability to move food from oropharynx via UES → esophagus
Drooling, postnasal regurgitation, difficulty initiating swallowing, sialorrhea, sensation of food stuck in the neck, coughing/choking during swallowing, dysphonia, and dysarthriaDiagnosis
First test = modified barium swallow videofluoroscopy, then fiberoptic flexible nasopharyngeal laryngoscopyb. Esophageal Dysphagia
Inability to move food from esophagus → stomach
Dysphagia to solids suggests mechanical obstruction.
Neuromuscular causes result in dysphagia to both solids and liquids.
Sx intermittent in pts with esophageal dysphagia from benign causes of structural obstruction or diffuse esophageal spasm; sx progressive in pts with peptic stricture, esophageal carcinoma, scleroderma, and achalasia
Luminal diameter >18 to 20 mm (rarely sx); diameter <13 mm (sx)Diagnosis
Esophageal dysphagia: first test = barium esophagography, then EGDTreatment
Goal is airway protection and nutrition maintenance.
Consider consultation with ENT, head and neck surgeon, radiologist, speech pathologist, physical therapist, dietitian, gastroenterologist, physical medicine and rehabilitation specialist, dentist, neurologist, etc., because nursing home pts with oropharyngeal dysphagia and hx of aspiration have 45% mortality rate over 1 yr2. Esophageal Motility Disorders
Table 6-1 compares esophageal motor disorders.TABLE 6-1
Esophageal Motor Disorders
| Achalasia | Scleroderma | Diffuse Esophageal Spasm | |
| Symptoms | Dysphagia Regurgitation of nonacidic material |
Gastroesophageal reflux disease Dysphagia |
Substernal chest pain (angina-like) Dysphagia with pain |
| Radiographic appearance | Dilated, fluid-filled esophagus Distal bird-beak stricture |
Aperistaltic esophagus Free reflux Peptic stricture |
Simultaneous noncoordinated contractions |
| Manometric Findings | |||
| Lower esophageal sphincter | High resting pressure Incomplete or abnormal relaxation with swallow |
Low resting pressure | Normal pressure |
| Body | Low-amplitude, simultaneous contractions after swallowing | Low-amplitude peristaltic contractions or no peristalsis | Some peristalsis Diffuse and simultaneous nonperistaltic contractions, occasionally high amplitude |
From Andreoli, T E, Benjamin IJ, Griggs RC, Wing EJ: Andreoli and Carpenter’s Cecil Essentials of Medicine, 8th ed. Philadelphia, Saunders, 2010.
3. GERD
Motility disorder caused by the reflux of gastric contents into the esophagusEtiology
Incompetent LES
Medications ↓ LES pressure (CCBs, β-blockers, theophylline, anti-AChs)
Foods ↓ LES pressure (chocolate, yellow onions, peppermint)
Tobacco abuse, alcohol, coffee
Pregnancy
Gastric acid hypersecretion
Hiatal hernia (present in 70% w/GERD ); however, most w/hiatal hernia asxDiagnosis
H&P
Heartburn, dysphagia, sour taste, regurgitation of gastric contents into mouth, chronic cough/bronchospasm, chest pain, laryngitis, early satiety, abd fullness and bloating w/belching, dental erosions in childrenAdditional Testing
EGD = document type/extent tissue damage; r/o potential malignancy (Barrett’s esophagus)
24-hr esophageal pH monitoring: generally not done; useful in atypical manifestations of GERD (chest pain and chronic cough)
Esophageal manometry: useful in refractory reflux pt w/surgical Rx planned
Upper GI series: identify ulcerations/strictures; may miss mucosal abnormalities. Only one third of pts w/GERD have radiographic signs of esophagitis.Treatment
Lifestyle change (wt loss, ↓ fat intake)/avoidance of exacerbating factors: EtOH, tobacco, citrus/tomato–based products, caffeine, β-blockers, CCBs, α-agonists, theophylline
↑ Head of bed 4 to 8 in. Avoid lying supine directly after late/large meals.
Avoid wearing clothing that is tight around the waist.
PPIs: preferred Rx (H2 blockers less effective)
Antacids: relief of mild sx; ineffective in severe cases
Prokinetic agents (metoclopramide): indicated if PPIs not fully effective. May be used in combination Rx; however, side effects limit use.
Nissen fundoplication (refractory cases)
Endoscopic radiofrequency heating of GE-jxn (Stretta procedure): pts unresponsive to traditional Rx4. Barrett’s Esophagus
Squamous lining of lower esophagus replaced by intestinalized metaplastic columnar epithelium; predisposing to neoplasiaH&P
Diagnosis
EGD with biopsyTreatment
Control GERD sx; maintain healed mucosa via PPIMonitoring
Relative risk of adenocarcinoma is 11.3 compared with general population.
Pts should undergo surveillance EGD and systematic four-quadrant biopsy at intervals determined by the presence and grade of dysplasia.
Pts who have had two consecutive EGDs showing no dysplasia should have follow-up every 3 to 5 yr.
Pts with low-grade dysplasia should have extensive mucosal sampling within 6 mo and follow-up every 6 to 12 mo.
Pts with high-grade dysplasia should have expert confirmation and extensive mucosal sampling. High-grade dysplasia with visible mucosal irregularities should be removed by endoscopic mucosal resection.
Consider intensive surveillance every 3 mo for patients with focal high-grade dysplasia. Patients with multifocal high-grade dysplasia or carcinoma should be considered for resection or ablation if not an operative candidate.5. Esophageal Tumors
15% in proximal third esophagus, 50% in middle third, 35% in lower third
Risk factors: EtOH, smoking, achalasia (7× > risk), chronic GERD, HPV (types 16, 18), obesity/hiatal hernia/low-vitamin high-fat diet, ingested carcinogens (nitrates, smoked opiates, fungal toxins [pickled vegetables], betel nut chewing), mucosal damage (long-term exposure tea >70° C, lye ingestion), radiation-induced strictureH&P
Dysphagia (74%): initially with solid foods; gradually → semisolids/liquids
Unintentional weight loss; losing >10% of body mass = poor outcome
Hoarseness (recurrent laryngeal nerve involvement)
Cervical adenopathy; usually supraclavicular lymph nodesDiagnosis
EGD
Endoscopic U/S: locoregional staging (depth of invasion/lymph assessment)
Chest/abd CT and/or integrated CT-PET scans (tumor spread for preop staging)
Staging laparoscopy may alter Rx plans (20%-30% cases) by more accurately staging regional lymph nodes/detecting occult peritoneal mets.Treatment
Surgical resection of squamous cell carcinoma and adenocarcinoma of lower esophageal third indicated for local, resectable disease in the absence of widespread mets detected by CT-PET. Gastric pull-through/colonic interposition is typically used to provide luminal continuity.
Squamous cell carcinoma is more radiosensitive than adenocarcinoma; used as palliative monoRx of obstructive sx in unresectable/advanced cases.
Palliative radiation Rx for bone mets
Preoperative chemoradioRx + surgery in late stage I (T2,3N0), stage II or III ↑ tumoricidal effects
5-yr survival 13% (37.3% [local], 18.4% [regional], 3.1% [distant] disease)C. Disorders of Stomach and Duodenum
1. Peptic Ulcer Disease
Etiology/Epidemiology
H. pylori infection (70%-90% duodenal ulcers)
NSAIDs (40%-50% gastric ulcers)
Cigarette smoking, EtOH
Neoplasia: gastrinoma (ZE syndrome), carcinoid, mastocytosisDiagnosis
EGD (preferred), UGI barium studies
Treatment
Lifestyle change: d/c smoking/EtOH.
Add PPI to ↓ acid secretions.TABLE 6-2
Overview of Antibiotics Used for Helicobacter Pylori Eradication
| Drug Class | Drug | Triple Therapy∗ Dose | Quadruple Therapy† Dose | Sequential Therapy‡ Dose |
| Acid suppression | Proton pump inhibitor | 20-40 mg bid§ | 20-40 mg bid§ | 20-40 mg bid§ |
| Standard antimicrobials | Bismuth compound|| | 2 tablets bid | 2 tablets bid | |
| Amoxicillin | 1 g bid | 1 g bid | ||
| Metronidazole¶ | 500 mg bid | 500 mg tid | 500 mg bid | |
| Clarithromycin | 500 mg bid | 500 mg bid | ||
| Tetracycline | 500 mg qid | |||
| Salvage antimicrobials | Levofloxacin | 300 mg bid | 300 mg bid | |
| Rifabutin | 150 mg bid | |||
| Furazolidone | 100 mg bid | |||
| Doxycycline | 100 mg bid | |||
| Nitazoxanide | 1 g bid |
∗ Triple therapy consists of a proton pump inhibitor or bismuth compound, together with two of the listed antibiotics, usually given for 7-14 days.
† Quadruple therapy consists of a proton pump inhibitor plus either the combination of a bismuth compound, metronidazole, and tetracycline given for 4-10 days, or the combination of levofloxacin, doxycycline, and nitazoxanide for 10 days.
‡ Sequential therapy consists of 10 days of proton pump inhibitor treatment, plus amoxicillin during days 1-5 and a combination of clarithromycin and an imidazole (when available, tinidazole; otherwise, metronidazole) during days 6-10.
§ Proton pump inhibitor dose equivalent to omeprazole 20 mg bid.
|| Bismuth subsalicylate or subcitrate.
¶ An alternative is tinidazole 500 mg bid.
From Goldman L, Schafer AI (eds): Goldman’s Cecil Medicine, 24th ed. Philadelphia, Saunders, Elsevier, 2012.
2. Gastroparesis
Sx impaired gastric emptying in absence of mechanical obstructionDifferential Diagnosis and Clinical Pearls
Diabetes mellitus gastroparesis (HBA1c, fasting glucose)
Gastric surgery
Pregnancy
Hypothyroidism (TSH)
Cannabinoid hyperemesis syndrome (hx of use; hx of relief of N/V with hot baths/showers)
Rumination syndrome (hx of passive regurgitation of pleasant tasting food w/o nausea)Management
Prokinetic agents (e.g., metoclopramide)
Refractory cases (↑ risk malnutrition), gastroduodenal manometry to distinguish myopathic from neuropathic process3. Gastric Cancer
Adenocarcinoma; mostly antral (35%)
Male-to-female ratio 3:2
Familiar diffuse gastric cancer (autosomal dominant, mutation E-cadherin gene CDH1 = cancer at young age)Physical Exam and Labs
Wt loss (70%-80%), N/V (20%-40%), dysphagia (20%)
Dyspepsia (unrelieved by antacids, worse w/food), epigastric/abd mass (40%)
Microcytic anemia, hemoccult (+) stools
HypoalbuminemiaDiagnosis
Upper endoscopy with biopsy (staging via abd CT scan ± lymph node dissection)
D. Disorders of the Pancreas
1. Acute Pancreatitis
Inflammatory process w/intrapancreatic enzyme activation possibly also involving peripancreatic tissue/remote organ systemsEtiology
>90% of cases: biliary tract disease (calculi or sludge) or EtOH
Drugs: thiazides, furosemide, corticosteroids, tetracycline, estrogens, valproic acid, metronidazole, azathioprine, methyldopa, pentamidine, ethacrynic acid, procainamide, sulindac, nitrofurantoin, ACEIs, danazol, cimetidine, piroxicam, gold, ranitidine, sulfasalazine, isoniazid, acetaminophen, cisplatin, opiates, erythromycin
Abd trauma, surgery, ERCP, viral infections, PUD, pancreas divisum (congenital failure to fuse of dorsal or ventral pancreas), pregnancy, vascular (vasculitis, ischemic), hypolipoproteinemia (types I, IV, and V), hypercalcemia, pancreatic carcinoma (primary/mets), renal failure, hereditary pancreatitis, occupational exposure (methanol, cobalt, zinc, mercuric chloride, creosol, lead, organophosphates, chlorinated naphthalenes)
Others: scorpion bite, obstruction at ampulla region (neoplasm, duodenal diverticula, Crohn’s disease), hypotensive shock, autoimmune pancreatitisScoring System
Table 6-3 describes various scoring systems to assess severity of acute pancreatitis.
TABLE 6-3
Scoring Systems to Assess Severity of Acute Pancreatitis
| System | Criteria |
| Ranson | At admission Age >55 yr WBC >16,000/μL Glucose >200 mg/dL LDH >350 IU/L AST >250 IU/L Within next 48 hr Decrease in hematocrit by >10% Estimated fluid sequestration of >6 L Serum calcium <8.0 mg/dL Pao2 <60 mm Hg BUN increase >5 mg/dL after hydration Base deficit >4 mmol/L |
| APACHE-II | Multiple clinical and laboratory factors. Calculator available at www.mdcalc.com/apache-ii-score-for-icu-mortality |
| BISAP | BUN >25 mg/dL Impaired mental status Presence of SIRS Age >60 yr Pleural effusion |
| CT | A: Normal pancreas B: Focal or diffuse enlargement of pancreas C: Grade B plus pancreatic and/or peripancreatic inflammation D: Grade C plus a single fluid collection E: Grade C plus two or more fluid collections or gas in pancreas |
| CT severity index | CT grade A = 0 B = 1 C = 2 D = 3 E = 4 Plus necrosis grade No necrosis = 0 <30% necrosis = 2 30-50% necrosis = 4 >50% necrosis = 6 |
APACHE-II, Acute Physiology and Chronic Health Evaluation II; BISAP, bedside index of severity in acute pancreatitis.
From Goldman L, Schafer AI (eds): Goldman’s Cecil Medicine, 24th ed. Philadelphia, Saunders, Elsevier, 2012.
“Severe Acute Pancreatitis”
The presence of any of the following 4 criteria:
1. Organ failure w/one or more of the following: shock (systolic BP <90 mm Hg), pulmonary insufficiency (Pao2 <60 mm Hg), renal failure (serum Cr >2 mg/dL after rehydration), and GI bleeding (>500 mL/24 hr)
2. Local complications such as necrosis, pseudocyst, or abscess
3. At least 3 of Ranson’s criteria
4. At least 8 of the APACHE II criteria
Diagnosis
H&P
Fever, epigastric tenderness/guarding; sudden severe pain (peak intensity 10-30 min; lasting several hr w/o relief)
Hypoactive bowel sounds (secondary to ileus)
Tachycardia, shock (secondary to ↓ intravascular volume)
Confusion (secondary to metabolic disturbances)
↓ Breath sounds (atelectasis, pleural effusions, ARDS)
Jaundice (secondary to obstruction or compression of biliary tract)
Ascites (secondary to tear in pancreatic duct, leaking pseudocyst)
Palpable abd mass (pseudocyst, phlegmon, abscess, carcinoma)
Hypocalcemia (Chvostek’s sign, Trousseau’s sign)
Intra-abd bleeding (hemorrhagic pancreatitis):• Gray-blue discoloration around umbilicus (Cullen’s sign)
• Bluish discoloration involving flanks (Grey Turner’s sign)
Tender SC nodules (SC fat necrosis)Labs
↑ Serum amylase (initial 3-5 days), ↑ serum lipase, ↑ serum trypsin
Rapid urinary trypsinogen-2; useful screening test in pts w/abd pain; (−) dipstick r/o acute pancreatitis w/high degree of probability; (+) test result indicates need for further evaluation.
CBC: leukocytosis; ↑ Hct (secondary to hemoconcentration); ↓ Hct may indicate hemorrhage/hemolysis.
↑ BUN (secondary to dehydration)
↑ Serum glucose; in previously nl pt correlates w/pancreatic malfunction
↑ AST/LDH (tissue necrosis); ↑ bili/alk phos (CBD obstruction); ≥3 ↑ ALT = biliary pancreatitis (95% probability)
↓ Serum Ca (saponification, precipitation, and ↓ PTH response)
ABGs: Pao2 may be ↓ secondary to ARDS, pleural effusions; pH may be ↓ secondary to lactic acidosis, respiratory acidosis, and renal insufficiency.
Serum electrolytes: K+ may be ↑ secondary to acidosis/renal insufficiency; Na+ may be ↑ secondary to dehydration.Imaging
Abd plain film: r/o perforated viscus; may reveal localized ileus (sentinel loop), pancreatic calcifications (chronic pancreatitis), blurring of left psoas shadow, dilation of transverse colon, calcified gallstones
CXR: elevation of one or both diaphragms, pleural effusions, basilar infiltrates, platelike atelectasis
Abd U/S: gallstones (sensitivity 60%-70%), pancreatic pseudocysts; limited in presence of distended bowel loops overlying pancreas
CT abd: superior to U/S in dx extent; also able dx pseudocysts (well-defined area surrounded by high-density capsule); GI fistulation or infection of a pseudocyst (gas within pseudocyst)
Contrast-enhanced CT (pancreatic necrosis): severity graded by CT scan (see Table 6-3)
MRCP: useful if surgical procedure not anticipated
ERCP: avoided during acute stage, unless to remove impacted stoneTreatment
General Measures
Maintain intravascular volume (vigorous IV hydration).
NPO until clinically improved, stable, and hungry; enteral feedings preferred to TPN; PN necessary if unable to tolerate enteral/adequate infusion rate cannot be reached within 2 to 4 days.
NG suction is used to decompress abd in pts w/ileus.
Control pain with IV morphine or fentanyl.
Specific Measures
Pancreatic/peripancreatic infection in 40% to 70% pts w/pancreatic necrosis; prophylactic IV abx (5-7 days) justified if septicemia, pancreatic abscess, or pancreatitis secondary to biliary calculi. Cover Bacteroides fragilis/anaerobes (cefotetan, metronidazole, clindamycin, + AG) and enterococcus (ampicillin).
Surgical Rx indicated: gallstone-induced pancreatitis (cholecystectomy when acute phase subsides), perforated peptic ulcer, excision/drainage necrotic/infected foci w/placement of wide-bore drains for continuous postop irrigationComplications
Pseudocyst (dx: CT scan or U/S) Rx: CT scan or U/S-guided percutaneous drainage w/pigtail catheter for continuous drainage (↑ recurrence rate); conservative approach to reevaluate (w/CT scan or U/S) after 6 to 7 wk and surgically drain if no ↓ in size. Pseudocysts <5 cm generally reabsorbed w/o intervention; those >5 cm require surgery after wall maturation.
Phlegmon (dx: CT scan or U/S) Rx: supportive care
Pancreatic abscess (dx: CT scan-retroperitoneal bubbles, Gram staining and cultures of fluid from percutaneous biopsy) Rx: surgical/catheter drainage + IV abx (imipenem-cilastatin)
Pancreatic ascites (dx: paracentesis-amylase/lipase level in fluid, ERCP) Rx: surgery if exudative/does not resolve spontaneously
GI bleeding: via EtOH gastritis, varices, stress ulcer, or DIC
Renal failure: via hypovolemia (oliguria or anuria), cortical or tubular necrosis (shock, DIC), or thrombosis of renal artery or vein
Hypoxia: via ARDS, pleural effusion, or atelectasis2. Chronic Pancreatitis
Recurrent/persistent inflammatory process characterized by chronic pain and pancreatic exocrine/endocrine insufficiencyEtiology
Chronic EtOH, obstruction (ampullary stenosis, tumor, trauma, pancreas divisum, annular pancreas), hereditary pancreatitis, severe malnutrition, untreated hyperparathyroidism (hypercalcemia), mutations of cystic fibrosis transmembrane conductance regulator (CFTR) gene (TF genotype)
Autoimmune (sclerosing) pancreatitis (5% cases): manifests w/jaundice (63%) + abd pain (35%). CT = diffusely enlarged pancreas, enhanced peripheral rim of hypoattenuation “halo,” and low-attenuation mass in head of pancreas. Labs = ↑ serum IgG4, serum Ig or γ -globulin level, + antilactoferrin Ab, anti–carbonic anhydrase II level, ASMA, or ANA.Diagnosis
H&P
Persistent/recurrent epigastric + LUQ pain, may radiate to the back
Tenderness over the pancreas, muscle guarding
Significant weight loss, epigastric mass (10%), jaundice (5%-10%)
Bulky/greasy, foul-smelling stoolsLabs
↑/Nl serum amylase and lipase
↑ Glucose, bili, alk phos, glycosuria
72-hr fecal fat determination (rarely performed) = excess fecal fat. Fecal elastase test requires 20 g of stool.
Secretin stimulation test (dx pancreatic exocrine insufficiency)
Lipid panel: ↑↑ TGs can cause pancreatitis.
Serum Ca: hyperparathyroidism (rare cause of chronic pancreatitis)
↑ Serum IgG4 (sclerosing pancreatitis and autoimmune pancreatitis)
↑ Serum Ig or γ-globulin level, antilactoferrin Ab, anti–carbonic anhydrase II level, ASMA, or ANA in autoimmune pancreatitisImaging
Plain abd radiographs: may reveal pancreatic calcifications (95% spec)
U/S abd: duct dilation, pseudocyst, calcification, presence of ascites
Contrast-enhanced abd CT scan: calcifications, evaluate ductal dilation, r/o pancreatic cancer
EUS (97% sens, 60% spec)
FNAB combined w/EUS = preferred evaluation of modality to r/o malignant cystic/mass lesions
Treatment
Steatorrhea Rx w/pancreatic supplements (e.g., pancrease, pancrelipase [Creon] PRN on basis of steatorrhea/weight loss)
Glucocorticoids (autoimmune pancreatitis)
Surgical intervention if duct obstruction
Transduodenal sphincteroplasty/pancreaticojejunostomy if intractable painClinical Pearls
50% of pts die within 10 yr of chronic pancreatitis or malignant neoplasm.3. Pancreatic Adenocarcinoma
Risk Factors
Smoking, chronic EtOH, genetics (5%-10% pts have family hx), dipeptidyl peptidase-4 inhibitors, incretin mimeticsDiagnosis
Labs: ↑ alk phos, bili, amylaseH&P
Jaundice, abd pain (dull upper abd pain/vague abd discomfort), wt lossImaging
Multidetector helical CT with IV contrast (imaging procedure of choice)
Endoscopic ultrasonography: useful if no identifiable mass on CT + ↑ clinical suspicionTreatment
Surgery
Curative cephalic pancreatoduodenectomy (Whipple’s procedure) in 10% to 20% pts whose lesion <5 cm, solitary, and without metastases. Surgical mortality rate is 5%.
Palliative surgery (for biliary decompression/diversion)
Palliative therapeutic ERCP with stents
Celiac plexus block = pain relief in 80% to 90% of casesChemoRx
Gemcitabine given alone or + platinum agent (erlotinib or fluoropyrimidine)
Combination consisting oxaliplatin, irinotecan, fluorouracil, and leucovorin (Folfirinox)Radiation
External-beam radiation for palliation of pain4. Neuroendocrine Pancreatic Neoplasms
a. Gastrinoma
ZE syndrome: hypergastrinemic state via pancreatic/extrapancreatic non–β islet cell tumor (gastrinoma) resulting in peptic ulcer disease
2/3 gastrinomas (sporadic), 60% assoc (MEN-1; AD including hyperparathyroidism, pituitary tumors)
60% gastrinomas = malignant (mets to liver, regional lymph nodes)
Neuroendocrine tumors = 1.3% of all cases of pancreatic cancerDiagnosis
Gastric acid secretion: serum gastrin level (fasting) >1000 pg/mL
Provocative gastrin level tests:• Secretin stimulation
• Ca2+ stimulation
Gastrinoma localization via arteriography, abd U/S or CT scan or MRI• Selective portal vein branch gastrin level
• Octreotide scan
H&P
95% sx of peptic ulcer, 60% sx related to GERD, 33% diarrhea, steatorrheaTreatment
Surgical resection; total gastrectomy/vagotomy (palliative in some pts)
Medical Rx: PPIs, somatostatin or octreotide, chemo (mets)b Insulinoma
Diagnosis
H&P
Sx typically in AM before meal; fasting hypoglycemia versus reactive hypoglycemia (which is not commonly associated w/insulinoma)Labs
Overnight fasting blood sugar level + simultaneous plasma insulin, proinsulin, and/or C peptide level will establish existence of fasting organic hypoglycemia in 60% of pts.
Plasma proinsulin, C-peptide, antibodies to insulin, and plasma sulfonylurea levels to r/o factitious insulin use/hypoglycemic agents/autoantibodies against the insulin receptor or insulin. Refer to Table 5-5 in Chapter 5.Imaging
Abdominal CT scan or MRI
Octreotide scanTreatment
Enucleation of single insulinoma
Partial pancreatectomy for multiple adenomasE. Disorders of Small and Large Bowel
1. Diarrhea
↑ Frequency (>200 g/24 hr) of stool w/ ↓ consistency compared with baseline; if lasting >3 wk = chronic diarrheaDiagnosis
Hx
Travel hx (traveler’s diarrhea)
Short duration (1-3 days) assoc w/mild sx usually viral (rotavirus, Norwalk virus); >3 wk probably not bacterial or viral
Nocturnal diarrhea (common w/diabetic neuropathy)
Onset within minutes: scombroid poisoning (tuna, mahi-mahi, mackerel) (N/V, flushing, diarrhea)
Onset within hr: toxins (Staphylococcus aureus, toxigenic Escherichia coli, Clostridium perfringens, Bacillus cereus, Vibrio parahaemolyticus, [barracuda, grouper, red snapper: ciguatera toxin, causing paresthesia, weakness])
Diarrhea secondary to Salmonella, Shigella, Campylobacter, Yersinia = longer incubation period.
Stress: “functional” diarrhea, IBS
Diarrhea alternating w/constipation: IBS
Foods containing sorbitol/mannitol (osmotic diarrhea), fried rice (B. cereus), undercooked hamburger (E. coli 157:H7), poultry, eggs (Campylobacter, Salmonella, S. aureus), diarrhea after dairy ingestion (lactose intolerance)
Shellfish ingestion (Norwalk virus, Vibrio cholerae, Vibrio mimicus, V. parahaemolyticus, Plesiomonas shigelloides)
Long-distance runners (bloody diarrhea secondary to bowel ischemia)
Daycare centers (rotavirus, Giardia, Salmonella, Shigella, Cryptosporidium, Campylobacter)
Medications: (common agents: Mg-containing antacids, misoprostol, PPIs, methylxanthines [caffeine, theophylline], laxatives, lactulose, colchicine, antiarrhythmic agents (quinidine, digitalis, propranolol), metformin, thyroxine). Abx-induced pseudomembranous colitis should be suspected in any pt receiving abx: (+) Clostridium difficile toxin w/the stool assay, cytotoxin test.
Sexual habits: male homosexuals ↑ incidence of (Giardia, E. histolytica, Cryptosporidium, Salmonella, Neisseria gonorrhoeae, Campylobacter).
Relevant medical hx• Surgical hx (ileal resection, gastrectomy, cholecystectomy), abd irradiation, DM, hyperthyroidism, watery diarrhea in elderly pts w/chronic constipation via fecal impaction/obstructing carcinoma
• AIDS: Cryptosporidium, Salmonella, CMV, Mycobacterium avium-intracellulare, Kaposi’s sarcoma involving the gut, AIDS enteropathy, Cyclospora spp (cyanobacterium-like bodies)
• Proteinuria, neuropathy: amyloidosis, DM
• Organ transplantation, cancer chemoRx, steroid Rx
Associated sx• Tenderness, fever, weight loss (IBD, amebiasis, lymphoma, tuberculosis)
• Abd pain + weight loss (carcinoma of pancreas/malignant neoplasia)
• Weight loss despite good appetite (malabsorption, hyperthyroidism)
• Diarrhea and PUD (ZE-syndrome, gastrinoma, gastrocolic fistula)
• Flushing and bronchospasm (carcinoid syndrome)
• LLQ pain, fever and/or bloody diarrhea (diverticulitis)
• Arthritis (IBD, Whipple’s disease)
• Bloody diarrhea, HUS, thrombocytopenic purpura (E. coli O157:H7)
Characteristics of the stool (from pt’s hx)• Large, foul smelling (malabsorption)
• ↑ Mucus (IBS)
• Watery stools (psychosomal disturbances, fecal impaction, colon carcinoma, IBD or IBS, Cyclospora infection, pancreatic cholera [vasoactive intestinal peptide])
PE
Rectal fistulas, RLQ abd mass (Crohn’s disease)
Arthritis, iritis, uveitis, erythema nodosum (IBD)
Abd masses (neoplasms of colon, pancreas, or liver; diverticular abscess [LLQ mass], IBD)
Flushing, bronchospasm (carcinoid syndrome)
Buccal pigmentation (Peutz-Jeghers syndrome)
Pigmentation (Addison’s disease)
Ammoniac/urinary breath odor (renal failure)
Ecchymosis (vitamin K deficiency secondary to malabsorption, fat-soluble vitamins, celiac)
Fever (IBD, infectious diarrhea, lymphoma)
Goiter, tremor, tachycardia (hyperthyroidism)
Lymphadenopathy (neoplasm, lymphoma, tuberculosis, AIDS, Whipple’s disease)
Macroglossia (amyloidosis)
Kaposi’s sarcoma (AIDS)Initial Evaluation
Labs (may not be necessary in pts not appearing ill/dehydrated)• CBC: ↑↑ WBCs w/left shift (? infection); ↓ Hb/Hct levels (? anemia via blood loss); ↑ Hct (? dehydration)
• Serum electrolytes: hypokalemia (diarrhea), hypernatremia (dehydration), hyponatremia (ADH compensation)
• BUN, Cr may be ↑ via dehydration.
• ELISA stool antigen test if suspect Giardia
• Stool evaluation: most cases self-limited generally not necessary; stool cultures considered if pt febrile + bloody diarrhea or immunocompromised. If obtaining stool sample, consider:
• Occult blood ([+] IBD, bowel ischemia, some infection)
• Löffler’s alkaline methylene blue stain for fecal leukocytes ([+] inflammatory diarrhea via Salmonella, Campylobacter, Yersinia, Shigella, invasive E. coli, although low sensitivity).
• Bacterial cultures if bloody stool w/suspected infection (Salmonella, Shigella, Campylobacter, Yersinia, E. coli O157:H7); culture for N. gonorrhoeae active male homosexual pts
• Examine O&P; indirect hemagglutination test (Entamoeba histolytica) if suspect amebiasis and stool exam inconclusive.
• C. difficile toxin: r/o pseudomembranous colitis if receiving abx
• Modified Ziehl-Neelsen stain, acid-fast, or auramine stain in immunocompromised pts w/suspected Cryptosporidium infection
Abd x-rays indicated if abd pain or evidence of obstruction (r/o toxic megacolon, bowel ischemia; pancreatic calcifications = pancreatic insufficiency)Treatment
NPO, IV hydration, electrolyte abnl correction, d/c possible causative agents (antacids containing Mg, abx)
Antiperistaltic agents (diphenoxylate) used w/caution in pts suspected of IBD or infectious diarrhea; loperamide/bismuth subsalicylate helpful in mild cases
Persistent diarrhea + bacterial/parasitic organism ID, start abx:• Giardia: metronidazole, 250 mg tid × 7 to 10 days, or tinidazole, quinacrine
• E. histolytica: metronidazole, 750 mg tid × 10 days, + either iodoquinol (650 mg tid × 20 days) or paromomycin
• Shigella: ciprofloxacin (Cipro) 500 mg bid × 3 days, or azithromycin 500 mg qd × 3 days
• Campylobacter: azithromycin 500 mg qd × 3 days or erythromycin 500 mg qid × 3 days
• C. difficile: PO metronidazole or vancomycin
• Cyclospora: TMP-SMX-DS bid × 7 days
• Salmonella (in pts w/sickle cell, HIV, uremia, malignancy, prosthetic device, age <6 mo or >50 yr): Cipro 500 mg bid × 5 to 7 days or TMP-SMX 160 mg/800 mg bid × 5 to 7 days. Mild cases + low-risk pts = no Rx
• V. cholerae O1/O39: Cipro 750 mg × 1, or doxycycline 300 mg × 1, or TMP-SMX 160 mg/800 mg bid × 3 days
• Cryptosporidium: paromomycin 500 mg tid × 7 days (severe)
• Yersinia species: Cipro 500 mg bid × 7 days or TMP-SMX 160 mg/800 mg × 7 days
• Isospora species: TMP-SMX 160 mg/800 mg qid × 10 days, then bid × 3 wk
• Microsporidium species: albendazole 400 mg bid × >3 wk
• Salmonella HIV pts: amoxicillin 1 g tid × 3 to 14 days, Cipro 500 mg bid× 7 days, or TMP-SMX bid × 14 days
IBS Rx: psyllium (fiber products) + ↓ caffeine, chocolate, EtOH, stress; antispasmodics (dicyclomine, hyoscyamine) if resistant casesEvaluation of Pt w/Chronic or Recurrent Diarrhea
Etiology
Drug induced (including laxative abuse), IBS, lactose intolerance, IBD, malabsorption (mucosal/pancreatic insufficiency, bacterial overgrowth), parasitic infections (giardiasis, amebiasis), functional diarrhea, postsurgical (partial gastrectomy, ileal resection, cholecystectomy)
Endocrine disturbances: DM (↓ sympathetic input to the gut), hyperthyroidism, Addison’s disease, gastrinoma (ZE syndrome), VIPoma (pancreatic cholera), carcinoid tumors (serotonin), medullary thyroid carcinoma (calcitonin)
Pelvic irradiation, colonic carcinoma (villous adenoma)
Collagenous colitis (middle-aged woman, nl endoscopy, subepithelial acellular collagen band on sigmoid bx or right colon; sx resolution w/sulfasalazine alone or steroid combination)
Lymphocytic colitis (lymphocytic infiltration w/o collagen band)Diagnosis
H&P/initial labs same as new-onset diarrhea; additional labs:• Sudan III stool stain: presence of fat droplets and meat fibers = malabsorption
• CBC = macrocytic, obtain vitamin B12 + RBC folate levels to r/o megaloblastic anemia secondary to malabsorption
• Mg-induced diarrhea dx w/quantitative fecal analysis for soluble Mg
• 24-hr urine for 5-HIAA if suspected carcinoid syndrome; serum gastrin level if suspected ZE syndrome
• Stool osmolality to evaluate for factitial diarrhea; hypotonic stools (? Munchausen syndrome/malingering because the colon does not excrete free water, hypotonicity indicates addition of water/urine/hypotonic fluid)
Secretory diarrhea from impaired absorption/excessive secretion of electrolytes via enteric infection, neoplasms of exocrine pancreas (VIP, GIP, secretin, glucagon), bile salt enteropathy, villous adenoma, IBD, carcinoid tumor, celiac, cathartic agent ingestion
Osmotic diarrhea from impaired water absorption secondary to osmotic effect of nonabsorbable intraluminal molecules via lactose and other disaccharide excess, pancreatic insufficiency, lactulose/sorbitol/sodium sulfate/antacid induced, postop (gastrojejunostomy, vagotomy, pyloroplasty, intestinal resection)
Dx “osmotic gap” in stool analysis = measured osmolality –2([Na+] + [K+])
Difference between calculated and actual Osm >50 = osmotic diarrhea2. Constipation
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