ICU Prophylaxis & Hospital-Acquired Complications
The daily checklist that stops new harm in the ICU
Stress ulcer and VTE prophylaxis
Why stress ulcers form. In shock and critical illness, splanchnic hypoperfusion leaves the gastric mucosa ischemic and poorly defended against acid, producing erosions that occasionally bleed. Two eponyms persist: the Cushing ulcer of severe brain injury (vagally driven acid hypersecretion) and the Curling ulcer of major burns (hypovolemic mucosal ischemia).
Who gets prophylaxis. Only high-risk patients: mechanical ventilation for more than 48 hours, coagulopathy (platelets <50,000/μL or INR >1.5), shock, severe traumatic brain or spinal cord injury, burns over 35% of body surface area, or GI bleeding within the past year. Low-risk patients gain only side effects.
Which agent. A PPI (pantoprazole) or an H2 blocker (famotidine); PPIs suppress acid more and prevent more clinically important bleeding. Acid suppression is associated with C. difficile infection and pneumonia, reflecting bacterial overgrowth in a less acidic stomach and microaspiration. Stop prophylaxis when the risk factors resolve, and do not continue it at transfer or discharge without a separate indication.
VTE prophylaxis. Immobility, central lines, sepsis, vasopressors, and surgery make venous thromboembolism common in the ICU, so nearly every patient needs prophylaxis; the only question is which kind.
| Option | Typical regimen | Best use | Caveats |
|---|---|---|---|
| LMWH | Enoxaparin 40 mg SC daily | Default for most patients | Renally cleared: avoid or reduce to 30 mg daily if CrCl <30 mL/min; lower HIT risk |
| Unfractionated heparin | 5,000 units SC every 8–12 h | Severe renal failure (CrCl <30) | Not renally cleared; higher HIT risk; fully reversed by protamine |
| Intermittent pneumatic compression | Sequential sleeves on both legs | Active bleeding or very high bleeding risk | Switch to an anticoagulant once bleeding risk passes |
Aspirin is not ICU VTE prophylaxis, and an IVC filter is not a substitute for prophylaxis; filters are reserved for proven VTE when anticoagulation is impossible.
Glucose control and nutrition
Glycemic target. Stress hyperglycemia impairs immunity and wound healing, but overtreatment is worse. Start an IV insulin infusion when glucose stays above 180 mg/dL and aim for 140–180. In the NICE-SUGAR trial, tight control (about 80–110 mg/dL) caused more severe hypoglycemia and higher 90-day mortality. Sliding-scale insulin alone is inadequate.
Enteral first. Begin enteral nutrition within 24–48 hours once the patient is hemodynamically stable, meaning not on escalating vasopressors. Feeding the gut preserves mucosal integrity and causes fewer infections than parenteral nutrition. Start gastric feeding and move postpyloric only for intolerance or high aspiration risk. Absent bowel sounds are no reason to wait, and gastric residual volumes are no longer measured routinely.
Parenteral nutrition. Reserved for patients who cannot be fed enterally: start early if severely malnourished, otherwise after about 7 days. It adds line infection, hyperglycemia, and cholestasis.
Refeeding syndrome. In malnourished patients (anorexia nervosa, alcohol use disorder, minimal intake for more than 5 days), carbohydrate triggers an insulin surge that drives phosphate, potassium, and magnesium into cells. Hypophosphatemia depletes ATP, causing respiratory muscle weakness and failed weaning, heart failure, arrhythmia, rhabdomyolysis, and hemolysis. Carbohydrate metabolism also consumes thiamine, so glucose without it can precipitate Wernicke encephalopathy. Prevent it: thiamine before feeding, start at 10–20 kcal/kg/day, advance slowly, and replace electrolytes.
Device-associated infections
CLABSI insertion bundle.
- Hand hygiene and a checklist, with authority for any team member to stop the procedure
- Maximal sterile barrier precautions: cap, mask, sterile gown, sterile gloves, full-body drape
- Chlorhexidine-alcohol skin antisepsis
- Ultrasound guidance
- Avoid the femoral vein in adults; the subclavian site has the lowest infection risk but the most pneumothorax
Maintenance. Review line necessity every day and remove unneeded catheters promptly. Use chlorhexidine dressings and daily chlorhexidine bathing and disinfect hubs before access. Do not replace catheters on a schedule or exchange them over a guidewire to prevent infection, but replace lines placed emergently without full asepsis within 48 hours.
Suspected CLABSI. Draw paired blood cultures from the catheter and a peripheral vein; growth from the line at least 2 hours earlier implicates the catheter. Common organisms are coagulase-negative staphylococci, S. aureus, enterococci, gram-negative rods, and Candida. Start empiric vancomycin (plus gram-negative coverage if septic or neutropenic) and remove the line for S. aureus, Pseudomonas, or Candida, or for persistent bacteremia.
CAUTI. Bacteriuria risk rises with every catheter day, so prevention centers on avoiding unnecessary catheters and removing them early through daily review and nurse-driven protocols, with aseptic insertion and a closed system draining below the bladder. Do not screen for or treat asymptomatic bacteriuria in catheterized patients; exceptions are pregnancy and urologic procedures that breach the mucosa. Candiduria usually reflects colonization and resolves with catheter removal.
ICU-acquired weakness
Presentation. Survivors of sepsis and multiorgan failure may wake with symmetric, flaccid limb weakness, reduced reflexes, and failure to wean from the ventilator, while facial and eye muscles are spared. Risk factors are sepsis, corticosteroids combined with neuromuscular blockers, hyperglycemia, immobility, and prolonged ventilation.
| Feature | Polyneuropathy (CIP) | Myopathy (CIM) |
|---|---|---|
| Lesion | Axonal sensorimotor nerve degeneration | Primary muscle injury with loss of myosin |
| Weakness | Distal more than proximal | Proximal more than distal |
| Sensation | Reduced | Intact |
| Nerve studies | Low motor (CMAP) and sensory (SNAP) amplitudes; normal velocity | Low CMAP, normal SNAP |
| CK | Normal | Normal or mildly raised |
| Recovery | Slower, often incomplete | Usually better |
Diagnosis and management. The diagnosis is clinical, an MRC sum score below 48/60 on bilateral testing of six muscle groups, supported by nerve conduction studies and EMG. Exclude Guillain-Barré syndrome (demyelinating, high CSF protein), myasthenia gravis, cord lesions, and severe hypophosphatemia or hypokalemia. There is no specific therapy: early mobilization, glucose control, and minimal steroids, paralytics, and sedation; recovery takes weeks to months.
Pressure injuries and the daily checklist
| Stage | What you see |
|---|---|
| Stage 1 | Intact skin with nonblanchable erythema |
| Stage 2 | Partial-thickness loss with exposed dermis, or an intact or ruptured serous blister |
| Stage 3 | Full-thickness skin loss with visible fat; no bone, tendon, or muscle |
| Stage 4 | Exposed or palpable bone, tendon, muscle, fascia, or cartilage |
| Unstageable | Base obscured by slough or eschar |
| Deep tissue injury | Intact skin with persistent purple or maroon discoloration or a blood blister |
Prevention. Score risk with the Braden scale, reposition at least every 2 hours, use pressure-redistributing mattresses, float the heels, control moisture and incontinence, optimize nutrition, and limit shear by keeping the head of the bed at or below 30° when possible. Check the sacrum, heels, ischium, occiput, and skin under tubes and masks.
Treatment. Offload pressure, use moist wound care, debride necrotic tissue, and look for osteomyelitis beneath stage 4 wounds. A stable, dry, adherent heel eschar is left intact as a natural biologic cover.
FAST HUGS BID. A daily rounding checklist ties these steps together: feeding, analgesia, sedation, thromboprophylaxis, head-of-bed elevation, ulcer prophylaxis, glucose control, spontaneous breathing trial, bowel regimen, indwelling catheter removal, and de-escalation of antibiotics.