Internal Bleeding + Shock (Hemorrhagic/Hypovolemic Shock) - Quick Summary

Key point on volume loss vs. signs

• ~10% blood loss: almost no change in BP/CO (compensated)
• ~15-20% loss without intact reflexes can be fatal; with intact sympathetic reflexes the body tolerates 30-40% loss before collapse
• 40-45% loss: CO and BP fall toward zero (Guyton, p. 2152-2159)

Classic clinical signs (internal bleeding + shock)

• Tachycardia, weak/rapid pulse
• Hypotension (late sign - appears only after significant loss because sympathetic vasoconstriction compensates first)
• Cold, clammy, pale skin (peripheral shutdown - blood shunted to brain/heart)
• Anxiety/confusion → decreasing consciousness as perfusion worsens
• Tachypnea
• Falling urine output
• Distension/pain/rigidity or a palpable mass if bleeding is intra-abdominal or pelvic; persistent shock despite fluid resuscitation with a falling hematocrit strongly suggests ongoing internal bleeding even without visible blood loss (Park's Preventive & Social Medicine; Pye's Surgical Handicraft, p. 1186).

Mechanism (compensation)

Management priorities

1. ABC - airway, oxygen, two large-bore IVs
2. Identify and stop the source of bleeding - this is the definitive treatment; fluids alone do not fix ongoing hemorrhage (surgery, endoscopy, embolization as indicated)
3. Volume resuscitation - crystalloids initially, early blood products (packed RBCs, plasma) for significant hemorrhage; avoid over-resuscitation with crystalloid alone in trauma
4. Identify occult sources - suspect internal bleeding when shock persists/hematocrit keeps falling despite resuscitation; use FAST/CT/serial exams to localize (pelvis, abdomen, chest, retroperitoneum, GI tract)
5. Monitor - vitals, urine output, mental status, lactate/hematocrit trend
6. Treat the underlying injury/disease definitively once identified

Diagnosing GI Bleeding as the Source of Internal Bleeding + Shock

1. History & clinical clues

• Hematemesis (vomiting fresh blood) or coffee-ground emesis → active/recent upper GI bleed (proximal to ligament of Treitz)
• Melena (black, tarry, foul-smelling stool) → usually upper GI bleed, but can be from small bowel/right colon
• Hematochezia (bright red/maroon blood per rectum) → usually lower GI bleed, but ~10% of hematochezia is actually a brisk upper GI bleed (blood transits too fast to become melena) - Tintinalli's Emergency Medicine, p. 3115
• Ask about NSAID/anticoagulant use, alcohol/liver disease, known varices/ulcers, prior GI bleeds, weight loss, abdominal pain

2. Exam

• Vitals for shock (tachycardia, hypotension, orthostatic drop)
• Abdominal exam - tenderness, mass, ascites, stigmata of liver disease (spider angiomata, jaundice → varices)
• Digital rectal exam - confirms melena/hematochezia, checks for mass

3. Labs

• CBC (Hb/Hct - note initial Hct may look normal before hemodilution catches up), coagulation panel/INR (INR ≥1.5 predicts higher mortality in upper GI bleed on anticoagulants), BUN/creatinine (disproportionately elevated BUN:Cr ratio suggests upper GI source from blood digestion), liver function tests, type & crossmatch, lactate

4. Bedside/early diagnostic steps

• NG tube lavage/aspirate: bloody or coffee-ground aspirate confirms upper GI source; a clear bilious aspirate makes upper GI bleed less likely but doesn't fully exclude it (e.g., duodenal bleed distal to pylorus)
• Rule out other internal bleeding sources first (abdominal exam, FAST/CT for trauma, pelvic/retroperitoneal causes) if the picture isn't classic for GI

5. Definitive diagnosis

• Upper endoscopy (EGD) - gold standard for upper GI bleed; done within 24 hours once hemodynamically stabilized; identifies and can treat ulcers, varices, Mallory-Weiss tears, Dieulafoy lesions
• Colonoscopy - for suspected lower GI bleed once bowel prepped/stable
• CT angiography - useful when bleeding is brisk/ongoing and endoscopy is not immediately available or non-diagnostic
• Tagged RBC scan or angiography - for obscure/intermittent bleeding, especially if endoscopy is negative; angiography also positive for active arterial bleeding and allows embolization
• Capsule endoscopy/enteroscopy - for suspected small bowel (obscure) bleeding when EGD and colonoscopy are negative

Key differentiator vs. non-GI internal bleeding

Diagnosing GI Bleeding When There's Blood Vomit (Hematemesis)

Step 1 - Confirm it's really GI bleeding

• Fresh red blood vomited = active, brisk bleeding
• Coffee-ground emesis (dark, granular) = blood that has been in contact with gastric acid for a while = slower or older bleeding
• Rule out mimics: swallowed blood from a nosebleed, dental extraction, or hemoptysis coughed up and then swallowed can look like hematemesis but isn't a GI source - Tintinalli's Emergency Medicine, p. 2957.

Step 2 - Use symptom pattern to narrow the cause

Step 3 - Assess severity (vitals over hemoglobin)

• Heart rate and BP are the most reliable early indicators - postural tachycardia/hypotension, then resting tachycardia, then hypotension as bleeding worsens
• Hemoglobin is misleading early on - it doesn't drop immediately because you lose whole blood (plasma and red cells proportionally); it can take up to 72 hours to fully reflect the loss. A "normal" Hb right after a big bleed does NOT rule out a serious bleed - Harrison's, p. 1538.
• Elevated BUN (disproportionate to creatinine) and hyperactive bowel sounds also support an upper GI source (digested blood protein raises BUN).

Step 4 - Risk-stratify

Step 5 - Confirm and localize with endoscopy

• Upper endoscopy (EGD) is the definitive test - done within 24 hours (sooner if unstable) - identifies ulcers, varices, tears, gastritis, and allows immediate treatment (clipping, banding, injection).
• NG tube aspirate: blood or coffee-ground return confirms an upper GI source right away at the bedside, before endoscopy.

When to worry it's NOT simple GI bleeding

Brown Blood - What It Means

Brown blood in vomit ("coffee-ground emesis")

• Vomit that looks dark brown/black with a grainy, coffee-ground appearance = blood that has sat in the stomach long enough for gastric acid to convert it to hematin
• Suggests bleeding that is slower or has slowed/stopped recently (as opposed to bright red hematemesis, which means active, brisk bleeding)
• Still indicates an upper GI source (stomach, duodenum, esophagus) - same workup applies (NG lavage, endoscopy within 24h) - Sleisenger and Fordtran's GI and Liver Disease, p. 1348; Frameworks for Internal Medicine, p. 335.
• Caution: iron supplements or red wine can also cause a coffee-ground-like appearance without true bleeding - S. Das Manual on Clinical Surgery, p. 608.

Dark brown, foul-smelling vomit ("faeculent vomiting")

• If the vomit is dark brown and smells like feces, this is different - it points to bowel obstruction (advanced low small bowel obstruction) or late peritonitis, where bowel contents mix with altered blood, not simple GI bleeding - S. Das Manual on Clinical Surgery, p. 586, 6381. This is a surgical emergency (obstruction/peritonitis), distinct from a bleeding ulcer or varix.

Brown blood in stool

• Normal stool is brown because of stercobilin (a bilirubin breakdown product) - this is completely normal, not bleeding - Rosen's Emergency Medicine, p. 2589.
• If you mean dark, tarry, black-brown stool with a strong odor - that's melena, which does indicate upper or right-colon GI bleeding that has been in the gut ≥14 hours.
• Bright red blood on/mixed with normal brown formed stool usually means a lower source (anal, rectal, sigmoid, e.g., hemorrhoids) - Harrison's Internal Medicine, p. 1272.

How endoscopy is typically done

• Conscious sedation (moderate sedation) - the most common approach. The patient is drowsy/relaxed but arousable and breathing on their own. This is fine for routine, stable patients - Bailey and Love's Short Practice of Surgery, p. 1103; Maingot's Abdominal Operations, p. 1579.
• Unsedated - some upper/lower endoscopies can even be done fully awake with no sedation at all.

When the patient is NOT conscious (or shouldn't be sedated lightly)

• General anesthesia with endotracheal intubation is used instead of conscious sedation when:
  • The patient is unconscious, obtunded, or has depressed mental status (common in massive GI bleeding with shock)
  • There's active, massive hematemesis or high risk of aspiration
  • The patient has severe comorbidities and can't safely tolerate conscious sedation
  • It's an emergency variceal bleed or unstable patient
  • Pediatric foreign body/impaction cases
• Fischer's Mastery of Surgery, p. 835: "Severe comorbidities and inability to tolerate conscious sedation preclude safe endoscopy [with sedation alone], although general anesthesia can be used in select cases."
• Barash, Cullen, and Stoelting's Clinical Anesthesia, p. 1870: "Under general anesthesia, tracheal intubation is the gold standard to protect the airway" during upper GI endoscopy.
• For a patient with obtunded mental status and massive hematemesis, guidelines (Washington Manual) specifically recommend intubation before endoscopy to protect the airway from aspiration.

Bottom line for your scenario (internal bleeding + shock)

Classification of Shock

1. Physiologic Classification (4 major types) - Harrison's Principles of Internal Medicine, Table 314-1

2. Severity Classification for Hemorrhagic/Hypovolemic Shock (ATLS - relevant to your internal bleeding scenario)

Why this matters for your case (internal bleeding + shock)

Hemorrhagic GI Bleeding - Detailed Overview

1. Classification (Anatomic)

2. Causes

• Duodenal ulcer, gastric ulcer (peptic ulcer disease - most common overall cause)
• Erosive gastritis/esophagitis
• Esophageal/gastric varices - due to portal hypertension in cirrhosis; can cause massive, life-threatening hematemesis
• Mallory-Weiss tear (mucosal tear from forceful vomiting/retching)
• Dieulafoy lesion (abnormally large submucosal artery - covered by normal mucosa, notoriously hard to find and treat)
• Angiodysplasia/AVMs, malignancy, duodenal diverticula

• Diverticulosis - single most common cause of LGIB, ~30% of cases
• Angiodysplasia/vascular ectasia - especially in older adults
• Colitis (ischemic, infectious, inflammatory bowel disease)
• Hemorrhoids, rectal varices
• Post-polypectomy bleeding
• Colorectal malignancy
• Radiation proctitis
• Meckel's diverticulum (pediatric - heterotopic gastric mucosa causes ileal ulceration)

3. Clinical Presentation

• Hematemesis / coffee-ground emesis → UGIB
• Melena (black, tarry, foul stool) → blood present ≥14 hrs in gut, usually UGIB or proximal source
• Hematochezia (bright red/maroon PR blood) → usually LGIB, but ~10% is actually a brisk UGIB
• Occult bleeding → no visible blood; presents as iron-deficiency anemia or positive fecal occult blood test

4. Pathophysiology of the Shock Component

5. Risk Stratification

6. Diagnostic Workup

1. Vitals + orthostatics (best initial assessment)
2. Labs: CBC, coagulation profile/INR, BUN/creatinine (elevated BUN:Cr ratio suggests UGIB), liver function tests, type & crossmatch, lactate
3. NG lavage - blood/coffee-ground aspirate confirms UGIB at bedside
4. Digital rectal exam - confirms melena/hematochezia
5. Endoscopy is the definitive diagnostic and therapeutic tool:
   • Upper endoscopy (EGD) within 24 hours for suspected UGIB
   • Colonoscopy (after prep) for suspected LGIB once stable
   • Capsule endoscopy/enteroscopy for obscure bleeding
6. CT angiography or tagged RBC scan / catheter angiography - for brisk/ongoing bleeding not localized by endoscopy, or when endoscopy isn't feasible (unstable patient); angiography also permits embolization

7. Management

• Airway protection - intubate first if obtunded/massive hematemesis (aspiration risk) before endoscopy
• Two large-bore IVs, crystalloid then blood products for ongoing/severe bleeding
• Restrictive transfusion threshold: Hb <7 g/dL (randomized trial evidence shows this reduces rebleeding and death vs. a 9 g/dL threshold) - Harrison's, p. 1538
• Reverse coagulopathy (INR ≥1.5 predicts higher mortality in UGIB on anticoagulants)

• IV proton pump inhibitor for suspected peptic ulcer/UGIB - reduces rebleeding, started empirically before endoscopy
• Octreotide/somatostatin analogue + prophylactic antibiotics if variceal bleeding suspected (cirrhotic patient)

8. Recent Evidence (last 2 years)

• Shung & Laine, Aliment Pharmacol Ther 2024 (PMID: 38517201) - review of current UGIB evidence, covers PPI use, endoscopic timing, and variceal management updates
• Ma et al., Korean J Intern Med 2024 (PMID: 38062723) - systematic review/meta-analysis on risk factors for anticoagulant-associated GI hemorrhage
• Xu et al., World J Pediatr 2025 (PMID: 41045337) - updated standardized approach to pediatric GI bleeding

Esophageal and Gastric Varices

What they are

Classification

• GOV1 (gastro-esophageal varix type 1): extends 2-5 cm below the gastroesophageal junction along the lesser curve, in continuity with esophageal varices - most common
• GOV2: extends into the fundus
• IGV1 (isolated gastric varix type 1): in the fundus, no esophageal varices
• IGV2: ectopic, elsewhere in the stomach

Presentation

• Sudden, often massive hematemesis (bright red, large volume)
• Melena
• Signs of chronic liver disease: jaundice, ascites, splenomegaly, spider angiomata, caput medusae
• Can rapidly progress to hemorrhagic shock given the volume and pressure behind variceal bleeds

Acute Management (variceal hemorrhage is a true emergency)

1. Resuscitate first: airway protection (intubate if massive hematemesis/altered mental status), IV access, blood products (restrictive transfusion, target Hb ~7-8 g/dL), correct coagulopathy
2. Vasoactive drugs started immediately, even before endoscopy: octreotide (or somatostatin/terlipressin where available) causes splanchnic vasoconstriction and reduces portal pressure/bleeding - Current Surgical Therapy, p. 689
3. Prophylactic antibiotics (e.g., ceftriaxone) - reduces infection risk and mortality in cirrhotic patients with GI bleeding
4. Endoscopy within 12 hours once stabilized:
   • Band ligation - preferred first-line therapy for esophageal varices, better than sclerotherapy for initial control - Sabiston Textbook of Surgery, p. 1791
   • Sclerotherapy - alternative, less preferred now
   • Cyanoacrylate (glue) injection - preferred for gastric varices, which don't respond as well to banding
5. Balloon tamponade (Sengstaken-Blakemore tube) - temporary bridge if bleeding uncontrolled by endoscopy, before definitive therapy
6. TIPS (transjugular intrahepatic portosystemic shunt) - salvage therapy for bleeding refractory to endoscopic + drug therapy; also superior to endoscopic therapy alone for preventing rebleeding long-term, though it carries a risk of hepatic encephalopathy - Yamada's Textbook of Gastroenterology, p. 2830

Prevention of rebleeding / primary prophylaxis

• Non-selective beta-blockers (propranolol, nadolol) reduce portal pressure and are used both for primary prophylaxis (known varices, not yet bled) and secondary prophylaxis (after a bleed), often combined with repeat band ligation sessions
• TIPS considered for recurrent bleeding despite combined drug + endoscopic therapy

Key distinction from other GI bleeds