Medical / GI / GU

• Severe abdominal pain (location guides differential — see below)
• Involuntary guarding and rigidity (peritoneal irritation)
• Rebound tenderness (pain increases when pressure is released)
• Absent bowel sounds (perforation/ileus) or hyperactive (early obstruction)
• Nausea, vomiting; fever in infectious causes
• Position of comfort: fetal position (peritonitis), or cannot find comfort (renal colic)

Location guides the differential: RUQ = cholecystitis (Murphy's sign — inspiratory arrest with palpation), RLQ = appendicitis (McBurney's point), periumbilical pulsatile mass + tearing pain = ruptured AAA. The AAA is the life threat — pulsatile mass + back pain + hypotension = immediate transport.

Elderly patient + abdominal pain + hypotension = ruptured abdominal aortic aneurysm until proven otherwise. AAA can present without a palpable mass. Do not delay transport for assessment — time to OR is the determining factor in survival.

• Upper GI: hematemesis (vomiting blood — bright red or coffee-ground appearance)
• Upper GI: melena (tarry, black, foul-smelling stool — digested blood)
• Lower GI: hematochezia (bright red blood from rectum)
• Tachycardia, hypotension in significant hemorrhage
• Pallor, weakness, syncope on standing (orthostatic)
• History: NSAID/aspirin use, alcoholism, cirrhosis, prior ulcer disease

Upper vs. lower GI bleed: Hematemesis or melena = upper source (esophageal varices, ulcer). Hematochezia = typically lower (hemorrhoids, diverticulosis, colitis). Melena can occasionally indicate a slow right-sided colon bleed. Hemodynamic instability is more common with upper GI bleeds.

Hematemesis + hemodynamic instability = massive upper GI bleed requiring urgent endoscopic intervention. Establish large-bore IV access and fluid resuscitation en route. Esophageal variceal bleeds carry a 20–30% in-hospital mortality.

• Fever (or hypothermia in severe/elderly — temp <36°C)
• Tachycardia; tachypnea
• Altered mental status (confusion, agitation, lethargy)
• Warm, flushed skin with wide pulse pressure — early distributive phase
• Cool, mottled skin — late decompensated phase
• Septic shock: hypotension unresponsive to IV fluid resuscitation

vs. Cardiogenic shock: Septic shock early has warm/flushed skin and wide pulse pressure. Cardiogenic shock has cool/clammy skin, JVD, and pulmonary edema. Critical distinction: fluids are aggressive in sepsis; cautious in cardiogenic. Do not conflate the two — wrong treatment worsens outcomes.

Septic shock mortality exceeds 40%. Lactate >2 mmol/L indicates tissue hypoperfusion even with normal BP. Aggressive IV fluids and early antibiotics within 1 hour (hospital) improve survival — field priority is recognition, IV access, and rapid transport.

• Polyuria (frequent urination) and polydipsia (excessive thirst)
• Kussmaul respirations: deep, rapid, sighing breaths (metabolic acidosis compensation)
• Fruity/acetone breath odor (ketone exhalation)
• Nausea, vomiting, abdominal pain
• Altered mental status (ranges from mild confusion to coma)
• Dehydration: dry mucous membranes, decreased skin turgor, tachycardia

vs. Hyperosmolar Hyperglycemic State (HHS): DKA occurs predominantly in Type 1 diabetics with ketoacidosis and moderate glucose elevation. HHS occurs in Type 2 elderly patients with extreme hyperglycemia (>600 mg/dL), no significant ketosis, and more profound AMS. Both require fluids; HHS patients are often more obtunded.

Kussmaul respirations are the body's compensation for metabolic acidosis. If these respirations STOP in an untreated DKA patient, it signals respiratory muscle fatigue — not improvement. Impending respiratory failure requires immediate airway management.

• Diaphoresis (most reliable early sign — adrenergic response)
• Tachycardia, tremor, anxiety, pallor
• Confusion, combativeness, bizarre behavior
• Focal neurological deficits that can be identical to stroke
• Seizure (severe, prolonged hypoglycemia)
• Blood glucose <60 mg/dL (field threshold for symptomatic treatment)

vs. Ischemic stroke: Hypoglycemia can produce focal neurological deficits, hemiparesis, and aphasia indistinguishable from stroke. Always check blood glucose before activating stroke protocol. Glucose <60 with neuro symptoms = treat hypoglycemia first; reassess if deficits persist after glucose correction.

Prolonged severe hypoglycemia causes irreversible neuronal death. Treat immediately with D50 IV (50 mL of 50% dextrose) or glucagon IM if no IV access. If the patient cannot protect their airway, do not give oral glucose — use IV or IM route only.

• AKI: decreased urine output, peripheral edema, hypertension
• AKI: nausea, fatigue, confusion (uremic encephalopathy in severe cases)
• Urinary Retention: severe lower abdominal/suprapubic pain
• Urinary Retention: palpable suprapubic mass (distended bladder)
• Urinary Retention: inability to void; agitation in elderly
• Risk factors: elderly men with BPH; post-operative; anticholinergic medications

AKI vs. Chronic kidney disease: AKI has a sudden onset with an identifiable precipitating cause (dehydration, infection, medications, obstruction). CKD develops gradually over months to years. Urinary retention causing back-pressure into the kidneys (post-renal AKI) is reversible if relieved promptly.

Uremic encephalopathy (AMS + severe AKI) indicates the need for emergent dialysis. Urinary retention with bladder volumes exceeding 500–1000 mL can cause bilateral hydronephrosis and permanent renal damage if not relieved — catheterization is definitive treatment.

• Urticaria (hives), pruritus, skin flushing
• Angioedema (lips, tongue, uvula, face)
• Hypotension and tachycardia (distributive shock — massive histamine release)
• Nausea, vomiting, diarrhea, abdominal cramping (GI involvement)
• Diaphoresis; sense of impending doom
• Known exposure: food (peanuts, shellfish), medications (PCN, contrast), venom, latex

vs. Vasovagal syncope: Vasovagal produces brief LOC with bradycardia (vagal), pallor, and diaphoresis — but NO skin findings (no urticaria or flushing) and NO sustained hypotension. Anaphylaxis has tachycardia + skin involvement + sustained hemodynamic compromise after a triggering exposure.

Biphasic anaphylaxis: symptoms can recur 4–12 hours after apparent resolution, even after epinephrine administration. All anaphylaxis patients require hospital observation regardless of symptom resolution in the field. Do not clear the scene after the patient "feels better."