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2025 PACUPrep BCCCP Preparatory Course Nausea, Vomiting & Gastrointestinal Symptoms Supportive Care and Monitoring of Nausea, Vomiting & Gastrointestinal Symptoms

Lesson 85, Topic 4

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Supportive Care and Monitoring of Nausea, Vomiting & Gastrointestinal Symptoms

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Supportive Care for Nausea, Vomiting & GI Symptoms

Supportive Care & Monitoring of Nausea, Vomiting & Gastrointestinal Symptoms

Lesson Objective

Recommend supportive care and monitoring strategies to manage complications associated with nausea, vomiting, and related GI symptoms in critically ill patients.

I. Airway Protection & Aspiration Prevention

Incessant vomiting compromises the airway and risks chemical pneumonitis or aspiration pneumonia. Early identification of lost protective reflexes and clear intubation criteria guide timely endotracheal tube placement. Post-intubation, ventilator-associated pneumonia (VAP) prevention bundles are critical.

1. Indications for Endotracheal Intubation

Glasgow Coma Scale ≤ 8 with risk of aspiration
Persistent, uncontrolled emesis with exhausted suctioning
Loss of cough/gag reflex or increasing oxygen requirement
Hemodynamic instability preventing safe noninvasive support

Key Pearl: Borderline Intubation Cases

In borderline cases (e.g., intermittent vomiting but intact reflexes), a trial of head-elevated noninvasive ventilation with aggressive suctioning may be appropriate. Reassess continuously for any signs of deterioration.

2. VAP Prevention Bundle Components

Maintain each element rigorously to cut ventilator-associated pneumonia (VAP) rates by approximately 50%:

Head-of-bed elevation to 30°–45°
Daily sedation interruption and spontaneous breathing trials
Oral hygiene with chlorhexidine every 12 hours
Subglottic secretion drainage via specialized endotracheal tube (ETT)
Stress ulcer prophylaxis (see Section III.B)

Clinical Pearl: Subglottic Suctioning

The use of endotracheal tubes with automated subglottic suction ports significantly reduces microaspiration and is particularly beneficial for patients expected to require intubation for more than 72 hours.

II. Volume Resuscitation & Hemodynamic Support

Volume depletion from vomiting leads to hypotension, tachycardia, and end-organ hypoperfusion. Dynamic predictors of fluid responsiveness and judicious choice of resuscitation fluid are key to optimizing outcomes.

1. Assessment of Dehydration/Hypovolemia

Clinical: Tachycardia, orthostasis, dry mucous membranes, decreased skin turgor.
Laboratory: BUN/Creatinine ratio > 20:1, rising hematocrit (hemoconcentration).
Dynamic Indices: Pulse pressure variation > 13% or stroke volume variation > 13% in mechanically ventilated patients.
Bedside Maneuvers: Passive leg raise (a reversible “self-challenge”), inferior vena cava (IVC) collapsibility on point-of-care ultrasound.

Key Pearl: Passive Leg Raise

The passive leg raise (PLR) maneuver predicts fluid responsiveness with approximately 80% sensitivity without requiring the administration of a fluid bolus. A positive response (e.g., >10% increase in stroke volume) strongly suggests the patient will benefit from fluids.

2. Crystalloids vs. Colloids: Selection & Titration

Comparison of Resuscitation Fluids
Fluid Type	Volume Effect	Acid–Base Impact	Renal Risk	Cost	Guideline Role
Balanced Crystalloids (LR, Plasma-Lyte)	100%	Neutral	Low	Low	First-line
0.9% Sodium Chloride	100%	Hyperchloremic Acidosis	Moderate	Low	Acceptable if brain injury risk
Albumin 5%–20%	150%–200%	Neutral	Low	High	Second-line for large volume needs
Synthetic Starches (HES)	100%–150%	Variable; ↑ Acidosis	High	High	Not Recommended

Pitfall: Synthetic Colloids

Hydroxyethyl starches (HES) have been shown to worsen acute kidney injury (AKI) and increase the risk of coagulopathy in critically ill patients. Their use for ICU resuscitation should be avoided.

III. ICU Prophylaxis Protocols

Critically ill patients with nausea and vomiting require prophylaxis against venous thromboembolism (VTE), stress ulcer bleeding, and nosocomial infections to reduce morbidity.

A. Venous Thromboembolism (VTE) Prophylaxis

Pharmacologic: Low-molecular-weight heparin (LMWH), such as enoxaparin 40 mg SC daily (or 30 mg SC q12h in trauma), is generally preferred over unfractionated heparin (UFH) for efficacy.
Renal Impairment (eGFR < 30 mL/min): Use UFH 5,000 units SC q8h or consider LMWH with anti-Xa monitoring if necessary.
Mechanical: Intermittent pneumatic compression devices are used when there is active bleeding or another contraindication to anticoagulation.

Clinical Pearl: Anti-Xa Monitoring

An anti-Xa peak level of 0.2–0.4 IU/mL can be used to guide enoxaparin dosing in patients with extremes of weight or moderate-to-severe renal dysfunction to ensure appropriate prophylactic effect.

B. Stress-Related Mucosal Bleeding Prophylaxis

High-Risk Criteria: Coagulopathy, shock, mechanical ventilation > 48 hours, high-dose steroid therapy.
Options: Proton pump inhibitors (e.g., pantoprazole 40 mg IV daily) or H2-receptor antagonists (e.g., famotidine 20 mg IV q12h).
De-escalation: Discontinue prophylaxis when risk factors resolve or as the patient approaches ICU discharge.

Pitfall: Overuse of PPIs

Routine use of proton pump inhibitors (PPIs) in low-risk patients is not recommended as it increases the risk of nosocomial pneumonia and Clostridioides difficile infection. Adhere strictly to guideline-based indications.

C. Infection Control & Antibiotic Stewardship

Standard Precautions: Rigorous hand hygiene and use of barrier precautions.
Device Care: Chlorhexidine oral care, limiting indwelling lines, and promoting early mobility.
Antimicrobial Stewardship: De-escalate antibiotics based on culture results and avoid prolonged broad-spectrum use.
Therapeutic Drug Monitoring (TDM): Use for renally cleared antibiotics like vancomycin and aminoglycosides to minimize toxicity.

IV. Management of Iatrogenic Complications

Antiemetics and supportive therapies can cause harm to the liver, kidneys, and electrolyte balance, as well as cardiac and neurologic function. Protocolized monitoring and correction algorithms are essential to mitigate these risks.

A. Drug-Induced Liver & Renal Dysfunction

TDM: Target vancomycin AUC/MIC ≥ 400 (troughs 15–20 µg/mL) and aminoglycoside peaks 8–10 µg/mL with troughs < 2 µg/mL.
Laboratory Monitoring: Check AST/ALT, bilirubin, and creatinine every 48–72 hours.
Dose Adjustments: Adjust doses based on creatinine clearance (CrCl) and clearance during continuous renal replacement therapy (CRRT).

Key Pearl: Vancomycin in CRRT

Continuous renal replacement therapy (CRRT) requires supplemental vancomycin dosing, particularly after filter changes, to maintain therapeutic AUC targets due to significant drug clearance by the circuit.

B. Electrolyte Disturbance Correction Algorithms

Electrolyte Replacement Protocols
Disturbance	Threshold	Replacement Regimen	Rate Limit
Hyponatremia	Na < 125 mEq/L + neuro symptoms	3% NaCl 1–2 mL/kg over 2 h	≤ 8 mEq/L per 24 h
Hypokalemia	K < 3.0 mEq/L	20–40 mEq KCl in 1 L crystalloid over 2–4 h	≤ 10 mEq/h (on cardiac monitor)
Hypomagnesemia	Mg < 1.2 mEq/L	MgSO₄ 1–2 g IV over 2 h	—
Hypophosphatemia	PO₄ < 1.0 mg/dL or symptomatic	0.08–0.16 mmol/kg IV over 4–6 h	—

Clinical Pearl: Refractory Hypokalemia

Always replete magnesium first in cases of refractory hypokalemia. Magnesium is a critical cofactor for the renal outer medullary potassium (ROMK) channel and Na-K-ATPase pump, facilitating intracellular potassium uptake.

C. Neurologic & Cardiac Safety Monitoring

QTc Prolongation: For antiemetics like 5-HT₃ antagonists, obtain a baseline and daily ECG. Institute continuous telemetry if the QTc exceeds 500 ms.
Extrapyramidal Symptoms (EPS): For dopamine antagonists like metoclopramide, assess the patient each shift using a dedicated scale. Treat acute dystonia promptly with diphenhydramine 25–50 mg IV.

Pitfall: EPS Assessment

Overreliance on symptom-driven assessment for extrapyramidal symptoms (EPS) may miss early, subtle signs like rigidity or akathisia. Use systematic screening tools to improve detection.

V. Multidisciplinary Goals of Care

Invasive supportive interventions for refractory nausea and vomiting carry significant burdens that may conflict with patient values. Early palliative care involvement and structured shared decision-making are crucial to align treatment with patient-centered goals.

1. Palliative & Ethics Consultations

Engage the palliative care team when considering prolonged intubation or artificial nutrition.
Clarify patient and family priorities, focusing on the balance between comfort and life-prolongation.

2. Shared Decision-Making for High-Burden Interventions

Clearly present the risks, benefits, and alternatives of continued mechanical ventilation, parenteral nutrition, and invasive device placement.
Diligently document advance directives, do-not-intubate (DNI) orders, and power-of-attorney preferences.

3. Communication & Documentation

Conduct regular, scheduled multidisciplinary family meetings to ensure consistent communication.
Use standardized forms to document goals of care, code status, and any limitations on treatment.

Key Pearl: Early Goals-of-Care Discussions

Proactive and early goals-of-care discussions have been shown to reduce non-beneficial ICU days, decrease family and clinician distress, and improve overall patient and family satisfaction with care.

References

Keyt H, Faverio P, Restrepo MI, et al. Aspiration in the intensive care unit: a narrative review. Crit Care. 2014;18(3):208.
Reinhart K, Bloos F, Brunkhorst FM, et al. Sepsis-3: an update. Intensive Care Med. 2016;42(4):521–530.
Kleiner SM. Fluid and electrolyte balance. World J Nephrol. 2019;8(1):23–29.
Schunemann HJ, Cushman M, Burnett AE, et al. American Society of Hematology 2018 guidelines for management of venous thromboembolism: prophylaxis for hospitalized and nonhospitalized medical patients. Blood Adv. 2018;2(22):3198–3225.
Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2024. Crit Care Med. 2024;(in press).
De Waele JJ, Roberts JA, Lipman J, et al. The choice of antibiotics in the critically ill. Intensive Care Med. 2020;46(5):1127–1153.
Lee JW. Fluid and electrolyte disturbances in critically ill patients. Electrolyte Blood Press. 2010;8(1):7–18.
Dipiro JT, Talbert RL, Yee GC, et al. Pharmacotherapy: A Pathophysiologic Approach. 11th ed. McGraw Hill; 2023.
Camilleri M, Parkman HP, Shafi MA, et al. Clinical guideline: management of gastroparesis. Am J Gastroenterol. 2013;108(1):18–38.
Abell TL, Camilleri M, Donohoe K, et al. Consensus recommendations for gastric emptying scintigraphy: a joint report of the American Neurogastroenterology and Motility Society and the Society of Nuclear Medicine. Am J Gastroenterol. 2008;103(3):753–763.
Parkman HP, Hasler WL, Fisher RS. American Gastroenterological Association technical review on the diagnosis and treatment of gastroparesis. Gastroenterology. 2004;127(5):1592–1622.
Heckroth M, Luckett RT, Moser C, et al. Nausea and vomiting in the critically ill. J Clin Gastroenterol. 2021;55(4):279–299.
Roila F, Molassiotis A, Herrstedt J, et al. 2016 MASCC and ESMO guideline update for the prevention of chemotherapy- and radiotherapy-induced nausea and vomiting and of nausea and vomiting in advanced cancer patients. Ann Oncol. 2016;27(suppl 5):v119–v133.

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