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Diarrhea, Acute Hemorrhagic 259
Diarrhea, Acute Hemorrhagic
VetBooks.ir Diseases and Disorders
• Loss of plasma water, electrolytes, and protein
BASIC INFORMATION
can be extreme. Packed cell volume (PCV) TREATMENT
Definition rises rapidly and often exceeds 65% (due to Treatment Overview
Acute, profuse hematemesis and hemorrhagic hemoconcentration). • Quickly restore and maintain an effective
diarrhea accompanied by hypovolemia; may • If untreated, hypovolemic shock and death circulating blood volume.
progress to circulatory collapse, multiple organ can occur. • Provide appropriate colloid support and
dysfunction, and death crystalloid fluid replacement.
DIAGNOSIS • Anticipate complications of hypovolemia and
Synonym widespread intestinal mucosal compromise.
Hemorrhagic gastroenteritis (HGE) Diagnostic Overview
A presumptive diagnosis is made based on Acute and Chronic Treatment
Epidemiology history and evidence of hemoconcentration • Initiate fluid resuscitation with IV fluid
SPECIES, AGE, SEX (PCV > 65%). Dogs with AHDS/HGE can therapy (p. 911).
Dogs, usually young (mean, 5 years old) die unless the disorder is recognized quickly ○ Colloids (e.g., Hetastarch, Vetstarch)
and treated intensively. It is important to rule should be started immediately in hypo-
GENETICS, BREED PREDISPOSITION out other possibilities, but treatment should volemic patients. Administer 5 mL/kg
Acute hemorrhagic diarrhea syndrome (AHDS) not be delayed while diagnostics are performed. over 20 minutes if the patient is sub-
can occur in any breed; small dogs may be stantially hypovolemic; otherwise, begin
predisposed. Differential Diagnosis a continuous-rate infusion of 1 mL/kg/h;
• Infectious gastroenteritis: viral (parvovirus) total daily dose should not exceed 20 mL/
CONTAGION AND ZOONOSIS or bacterial (Salmonella, Clostridium difficile, kg.
Does not appear to be contagious salmon poisoning [Neorickettsia helminthoeca] ○ Crystalloid fluids should be administered
in endemic regions) concurrently. Replacement-type fluids
GEOGRAPHY AND SEASONALITY • Dietary indiscretion, toxicity (e.g., Normosol-R, lactated Ringer’s solu-
More prevalent in urban dogs • Hypoadrenocorticism tion, Plasmalyte 148, 0.9% NaCl) should
• Intestinal volvulus, partial obstruction, or be used. If necessary, calculate a shock
Clinical Presentation intussusception dose of crystalloids (90 mL/kg), and give
HISTORY, CHIEF COMPLAINT • Other causes of hypovolemic or endotoxic one-third of this amount as a bolus over 20
• Anorexia and lethargy initially shock (e.g., intestinal perforation, peritonitis) minutes. Do not administer Normosol-R
• Acute onset of vomiting that may be profuse • Necrotizing pancreatitis rapidly because this fluid contains acetate
and contain fresh blood • Coagulopathy and may cause refractory hypotension.
• Acute onset of diarrhea that may become ○ Estimate lost volume (by % body weight)
grossly bloody; consistency varies from watery Initial Database and aim to replace over 6-12 hours.
to jelly-like. • PCV is often > 65%; total solids are low or ○ Continue fluids as needed to replace
borderline normal. ongoing losses and meet maintenance
PHYSICAL EXAM FINDINGS • CBC: stress leukogram; immature neutrophils requirements.
• Depressed but afebrile or mild toxic change may be noted; modest ○ If available, use COP measurement to
• Markers of perfusion: heart rate, pulse thrombocytopenia is common. guide colloid administration.
quality, gum color, capillary refill time • Serum biochemistry profile: increased blood • Electrolyte disturbances are common:
(CRT) initially normal. As fluid is urea nitrogen (BUN) level and alanine hypokalemia (p. 516) should be addressed
lost into the gastrointestinal (GI) tract, aminotransferase activity are expected; specifically; changes in sodium and chloride
signs of hypovolemia, characterized by hypokalemia and panhypoproteinemia are should self-correct with standard fluid
pallor, slow CRT, and tachycardia, quickly common; metabolic acidosis may be severe. therapy.
develop. • Urinalysis: unremarkable; high specific gravity • Antibiotics are of questionable benefit
• Skin turgor may not reflect the full extent expected in response to hypovolemia (despite evidence of an underlying Clostridial
of fluid losses. • Coagulation profile: usually normal initially; cause) unless the clinical assessment suggests
• Patients may be moribund at presentation may show prolongations if disseminated sepsis. If so, provide broad-spectrum cover-
if veterinary attention is delayed. intravascular coagulation (DIC) develops age (e.g., ampicillin 30 mg/kg IV q 8h and
• Abdominal palpation reveals fluid-filled • Fecal evaluation (centrifuged flotation and enrofloxacin 10 mg/kg slow IV q 24h).
bowel loops with nonlocalized discomfort. saline preparation): no pathogens noted • Antiemetics should be administered to
• Rectal examination: fresh dark blood or • Fecal stained microscopic exam: increased control vomiting.
strawberry jelly–like feces numbers of red cells, some white cells ○ Maropitant 1 mg/kg SQ q 24h (patient
• Fecal ELISA for parvovirus (if neonate or must be > 8 weeks old), or
Etiology and Pathophysiology unvaccinated): negative ○ Metoclopramide 1.1-2.2 mg/kg/24 hours
• A novel pore-forming toxin (NetF) from • Canine pancreas-specific lipase immunoassay given IV as constant-rate infusion)
type A Clostridium perfringens is the probable (cPLI): not consistent with pancreatitis • Gastric acid suppressing drugs are not
cause of AHDS/HGE. • Abdominal radiographs: fluid- and gas- specifically indicated but may reduce the
• GI permeability increases markedly, with filled small-intestinal loops; colon may be risk of esophagitis in patients with sustained
extravasation of fluid, proteins, and red empty emesis.
blood cells into the intestinal lumen. • Colloid oncotic pressure (COP): usually ○ Pantoprazole 0.7 mg/kg IV q 24h or
• Although vomiting (often with hematemesis) normal at presentation but then declines famotidine 0.5 mg/kg IV or SQ q 12-24h
is expected, the stomach is grossly and • +/− Serum cortisol > 2 mcg/dL (>55 nmol/L) • Probiotics/prebiotics may hasten recovery,
microscopically unaffected. excludes hypoadrenocorticism. but evidence to support their use is limited.
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