Reverse DOACs specifically when bleeding is life-threatening (idarucizumab for dabigatran, andexanet alfa for Xa inhibitors); 4-factor PCC for warfarin.
Pathways
First Steps in Acute Gastrointestinal (GI) Bleeding
Resuscitate: place two large-bore IVs or a central line · send blood for typing, CBC, CMP, INR, PTT · infuse isotonic saline or Ringer's lactate (hetastarch is harmful — never use) · transfuse O negative blood if extremely urgent · give oxygen only if hypoxemic
Factors propagating bleeding: stop anticoagulants (warfarin, heparin) and thrombolytic agents · temporarily withhold antiplatelet therapy after balancing bleeding risk against thrombotic risk, particularly with recent coronary stents or acute coronary syndrome (aspirin, clopidogrel) · stop antithrombotic agents if possible (glycoprotein IIb/IIIa receptor antagonists — abciximab, eptifibatide, tirofiban; direct thrombin inhibitors — argatroban, bivalirudin) · reverse warfarin with 4-factor PCC (weight/INR-based 25–50 IU/kg) + IV vitamin K — FFP only if PCC unavailable; reverse DOACs when life-threatening: idarucizumab (dabigatran), andexanet alfa (Xa inhibitors) · reverse unfractionated heparin with protamine (protamine provides only partial reversal of LMWH)
Bleeding level: hematemesis or coffee ground emesis points to upper GI bleeding · melena usually means upper GI bleeding but may arise more distally · maroon stool or red blood in the stool typically signals lower GI bleeding · any bleeding with hemodynamic compromise may still be upper GI in origin
Upper GI bleeding signs: blood or coffee grounds in NG tube aspirate · hematemesis (emesis of blood or coffee grounds) · melena · maroon or red blood in stool with hemodynamic compromise
Variceal versus nonvariceal bleeding? (clinical indicators)
VARICEAL — clinical clues: history of liver disease/cirrhosis · history of varices/variceal bleeding · ascites · spider angiomata · caput medusa · splenomegaly · hepatic encephalopathy · pancytopenia, low albumin
Resuscitate first: consider elective intubation for airway protection · balloon tamponade (e.g., Sengstaken–Blakemore tube) only as a temporary bridge (<24 h) until definitive endoscopic therapy or TIPS · blood pressure tends to run low in cirrhotic patients — beware over hydration and fluid overload
Drug therapy: octreotide bolus then infusion · IV ceftriaxone (preferred) for up to 7 days to prevent bacterial infection/SBP · vasopressin infusion is an alternative but side effects may be limiting; rarely used
Endoscopic therapy: endoscopic variceal ligation (preferred); sclerotherapy only when band ligation is not feasible · variceal band ligation · glue injection for gastric varices — repeatable if bleeding recurs
Angiography: consider early (pre-emptive) or rescue TIPS in selected high-risk patients, or when bleeding cannot be controlled endoscopically, for gastric varices from portal hypertension · TIPS placement when endoscopic therapy fails
Surgery: surgical shunts for portal hypertension · splenectomy for gastric varices due to splenic vein thrombosis
NONVARICEAL — clinical clues: no liver disease · history of peptic ulcers · history of Helicobacter pylori · history of retching/vomiting · NSAID/aspirin use · chronic renal disease · aortic stenosis (Heyde syndrome) · history of hereditary hemorrhagic telangiectasia
Resuscitate first → drug therapy: intravenous PPI bolus or infusion OR high-dose oral PPI bid once oral intake is tolerated
Endoscopic therapy: chosen by stigmata of recent bleeding
Angiography: when endoscopy fails or bleeding is too brisk for endoscopic localization and therapy
Surgery: reserved when endoscopic and/or angiographic therapy fails or is unavailable · neoplasms, benign and malignant · isolated vascular abnormalities, e.g., Dieulafoy lesion · aortoenteric fistula → emergent surgery
Managing Peptic Ulcers
Peptic ulcer disease: gastric and duodenal ulcers · gastric and duodenal erosions · gastritis
First-line management — PPI acid suppression: 8 wks for most gastric ulcers (longer if large, refractory, or not healed) · 8 wks for duodenal ulcers · 4–6 wks for erosions/gastritis
Further workup: Helicobacter pylori testing · NSAID/aspirin history
H. pylori: give eradication therapy · confirm H. pylori eradication in all treated patients
NSAID/aspirin ulcers: switch to a less toxic NSAID · stop the NSAID if possible · misoprostol for prophylaxis · continuous PPI prophylaxis · if NSAID therapy must continue, use a COX-2 inhibitor plus a PPI
Idiopathic: retest for H. pylori · scrutinize carefully for NSAID/aspirin use · check fasting serum gastrin when Zollinger–Ellison syndrome is suspected
Refractory H. pylori (still present after two courses of therapy): culture and sensitivity to guide antibiotic choice · continue PPI only if there is an ongoing indication (e.g., active ulcer or continued NSAID requirement)
Suspected gastrinoma: secretin stimulation test · gastric output analysis · Ga-68 DOTATATE PET/CT (preferred) ± CT/MRI/EUS for localization · surgery if localized · long-term PPI if refractory
Repeat upper endoscopy (with biopsy if not healed or suspicious) to confirm healing of gastric ulcers when indicated; when not fully healed, take multiple biopsies to exclude other nonpeptic causes, including malignancy
ICU Decoded — original critical-care and internal-medicine pathways by
Dr Javed Akhtar, each cited to a current guideline. For education and quick
reference; verify every dose against local protocols before prescribing.