The Acutely III Patient

11.1 Critical Illness

David Wang

Vivek K. Moitra

There are several preoperative challenges when patients who require intensive care need surgery. The critically ill patient can have complex and challenging physiologic changes ranging from electrolyte abnormalities to multiple organ failure and is thoroughly evaluated before surgery. This chapter reviews the preoperative assessment and management of critically ill patients via an organ system approach.

NEUROLOGIC

Pain and Analgo-Sedation

A significant number of critically ill patients experience pain at rest and during procedures, with an incidence of significant pain of 50% in medical and surgical intensive care unit (ICU) patients. Uncontrolled pain is associated with development of chronic pain, posttraumatic stress disorder, lower quality of life, decreased tissue perfusion, hypoxemia, increased catabolism, immunosuppression, and impaired wound healing (1,2,3).

Some mechanically ventilated patients do not require sedation or analgesia to tolerate an endotracheal tube.
Analgo-sedation should focus on analgesia first or an “A-1” approach before administration of sedation to prevent disinhibition when agitation is secondary to pain.
The Richmond Agitation-Sedation Scale (RASS) is a valid and reliable assessment tool for measuring depth of sedation (Table 11.1).
Light levels of sedation (RASS 0-1) are associated with reduced duration of mechanical ventilation and ICU length of stays.
If the patient is awake and alert, traditional pain scales such as the numerical rating scale are used to assess pain control.
The Behavioral Pain Scale (BPS) and Critical Care Pain Observation Tool (CPOT) can assess pain in patients who cannot self-report (4).

Delirium and Cognitive Impairment

The hallmark feature of delirium is inattention. Although the pathogenesis of delirium is poorly understood, alterations in neurotransmission (cholinergic deficiency and dopaminergic excess), inflammation, and stress are implicated (5). Sedatives,
narcotics, intracranial bleeding, meningitis, surgery, infections, severe acute illness, shock, fever, hypothermia, metabolic derangements, sleep deprivation, ICU admission, physical restraints, bladder catheter, pain, and procedures can precipitate delirium. The incidence of delirium occurs in up to 70% of ICU patients (1,2).

TABLE 11.1 The Richmond Agitation-Sedation Scale (RASS)

Score	Term	Description
+4	Combative	Overtly combative or violent; immediate danger to staff
+3	Very agitated	Pulls on or removes tube(s) or catheter(s) or has aggressive behavior toward staff
+2	Agitated	Frequent nonpurposeful movement or patient-ventilator dyssynchrony
+1	Restless	Anxious or apprehensive but movements not aggressive or vigorous
0	Alert and calm	Spontaneously pays attention to caregiver
-1	Drowsy	Not fully alert, but has sustained (>10 seconds) awakening with eye contact to voice
-2	Light sedation	Briefly (<10 seconds) awakens with eye contact to voice
-3	Moderate sedation	Any movement, but no eye contact to voice
-4	Deep sedation	No response to voice, but movement to physical stimulation
-5	Unarousable	No response to voice or physical stimulation
Copyright © 2013, E. Wesley Ely, MD, MPH and Vanderbilt University, all rights reserved.

The symptoms of delirium may be subtle and patients should be screened daily with standardized tools (i.e., the Confusion Assessment Method for the ICU [CAM-ICU]) (Fig. 11.1).
Delirium impacts history taking and informed consent, and the health care proxy or family members are included when possible (3).
Reversible etiologies of delirium (hypothyroidism, infection, medications, vitamin deficiencies, drug abuse, or withdrawal) need to be identified before surgery.
Benzodiazepines should be avoided if possible (1).

ICU-Acquired Weakness

ICU-acquired weakness (ICUAW) includes critical illness polyneuropathy and myopathy. The diagnosis of ICUAW is challenging because electromyography and nerve conduction studies are often not available. It may be assumed that some degree of ICUAW is present in all critically ill patients (incidence of 25% to 100%) (6).

Succinylcholine administration can cause life-threatening increases in serum potassium due to the proliferation of acetylcholine receptors in critically ill patients with prolonged immobilization.
Patients with ICUAW may be sensitive to nondepolarizing relaxants.
Critical illness polyneuropathy may increase the risk of neurologic injury from regional anesthesia although studies are limited (7).

INFECTIOUS DISEASE

There is a high rate of nosocomial infection, such as catheter-related blood stream infections (CRBSIs), catheter-associated urinary tract infections (CAUTIs), and Clostridium difficile infections. Sepsis is defined as life-threatening organ dysfunction due to dysregulated host response to infection and septic shock has an in-hospital mortality >40% (8).

Prevention of Infection

The use of maximal sterile barrier precautions must be observed for the placement of all central venous catheters (9).
Foley catheters are removed as soon as possible.
Clostridium difficile infections can be prevented with hand washing, antibiotic stewardship, and avoiding medications that change gastric pH (10).

Sepsis Evaluation

Septic shock is the presence of sepsis with persistent hypotension despite adequate volume resuscitation requiring vasopressors to maintain mean arterial blood pressure (MAP) ≥65 mm Hg with a lactate ≥2 mmol/L (8).
The quick Sequential (Sepsis-Related) Organ Failure Assessment (qSOFA) score is inadequate for the diagnosis of sepsis, but predictive of increased in-hospital mortality and useful for rapid assessment in the setting of limited data (Table 11.2) (8).
An increase in ≥2 points in the SOFA or an increase of 2 qSOFA points is associated with a mortality of 10% (Table 11.2) (8).

Sepsis Management

Surgery for source control of an infection should not be delayed.
Microbiology investigations guide appropriate antibiotic (empiric or prescriptive) therapy expeditiously.
Mortality is increased when antibiotics are delayed (11).
Assess fluid responsiveness prior to induction of anesthesia via fluid boluses (250 to 500 mL) or passive leg raise.
If hemodynamics do not improve after initial fluid resuscitation, norepinephrine is the preferred initial vasopressor, followed by epinephrine or vasopressin (8).
Dobutamine is considered for sepsis-induced myocardial dysfunction (12).
Provide lung protective ventilation per the ARDSnet protocol (discussed below).

CIRCULATORY

Shock occurs when inadequate tissue perfusion causes cellular injury or dysfunction. Vasodilation, hypovolemia, obstruction to flow, and cardiac dysfunction compromise the circulation and cause shock. These mechanisms are not mutually exclusive.

The type of shock is determined by physical examination, hemodynamic monitoring, and echocardiography. Lactate levels are nonspecific to differentiate among types of shock.

TABLE 11.2 Sequential (Sepsis-Related) Organ Failure Assessment (SOFA) and Quick SOFA (qSOFA)

SOFA Score	0	1	2	3	4
Respiratory PaO₂/FiO₂ (mm Hg)	>400	<400	<300	<200	<100
Coagulation Platelets 10³/µL	>150	<150	<100	<50	<20
Liver Bilirubin (mg/dL)	<1.2	1.2-1.9	2.0-5.9	6.0-11.9	>12.0
Cardiovascular Hypotension^adoses of drugs (µg/kg/min)	No hypotension	MAP <70 mm Hg	Dopamine ≤5^a or dobutamine (any dose)	Dopamine >5^a or norepinephrine ≤0.1^a	Dopamine >15^a or norepinephrine >0.1^a or epinephrine >0.1^a
CNS GCS	15	13-14	10-12	6-9	<6
Renal Creatinine (mg/dL) or UOP	<1.2	1.2-1.9	2.0-3.4	3.5-4.9 <500 mL/day	>5.0 <200 mL/day
qSOFA			1 Point
Hypotension			SBP ≤100 mm Hg
Altered mental status			Any GCS <15
Tachypnea			RR ≥22
For patients with infections, an increase of 2 SOFA points predicts an overall mortality rate of 10%. ^aDoses are given in mcg/kg/min. PaO₂, partial pressure of oxygen; FiO₂, fraction of inspired oxygen; CNS, central nervous system; UOP, urine output; GCS, Glasgow Coma Score; SBP, systolic blood pressure; RR, respiratory rate Adapted from Vincent JL, Moreno R, Takala J, et al. The SOFA (sepsis-related organ failure assessment) score to describe organ dysfunction/failure. Intensive Care Med. 1996;22:707-710.; Singer M, Deutschman CS, Seymour CW, et al. The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA. 2016;315:801-810.

Vasodilation is associated with a wide pulse pressure, warm extremities, and a hyperdynamic left ventricle.
Hypovolemia is associated with a narrow pulse pressure, cool extremities, and an underfilled left ventricle.
Cardiogenic shock is associated with a narrow pulse pressure, cool extremities, and impaired myocardial contractility or relaxation.
Sepsis, inflammatory responses, liver failure, adrenal insufficiency, neurogenic shock, and anaphylaxis cause vasodilation. These conditions are managed with fluid resuscitation and vasopressor therapy.
Norepinephrine and vasopressin synergistically treat vasodilation.
Sepsis-induced cardiomyopathy is suspected if inadequate cardiac output (CO) despite adequate fluid resuscitation is present (13).
Catecholamine release in the setting of physical or emotional stress can cause a Takotsubo cardiomyopathy in patients with no prior history of cardiac disease and a noncardiac primary diagnosis with a reported incidence as high as 28% (14) (see Chapter 3.16).
A Takotsubo cardiomyopathy can be associated with left ventricular outflow tract (LVOT) obstruction (15).

RESPIRATORY/MECHANICAL VENTILATION

Mechanical ventilation is indicated for respiratory failure. Hypoxemia, hypercarbia, postoperative etiologies, shock, pneumonia, pulmonary edema, and ARDS cause respiratory failure.

TV are based on ideal body weight (IBW), not total body weight.
TV are set at 6 to 8 cc/kg (IBW) and adjusted accordingly.
A plateau pressure is measured before surgery to assess respiratory system compliance.
TV and respiratory rate are maintained during transport.
Patients with chronic obstructive pulmonary disease (COPD) and asthma are at risk for auto-PEEP, which may cause hypotension.
Consider performing surgery in the ICU if the patient has high FiO₂ or PEEP requirements.
Severity of ARDS is stratified based on the PaO₂/FiO₂ ratio, with 200 to 300 considered mild, 100 to 200 moderate, and <100 severe (16).
In ARDS, measures to limit transpulmonary pressures with target TV of 6 mL/kg (IBW) and plateau pressures <30 cm H₂O are goals (17).
Recruitment maneuvers, inhaled nitric oxide (iNO) or prostacyclin, and extracorporeal membrane oxygenation (ECMO) are considered for refractory hypoxemia. Data are not robust for these strategies, but they may be warranted in the setting of refractory hypoxemia when emergency surgery is required (18).

RENAL

AKI is a continuum of injury classified by several scoring systems (see Chapter 6.3).

Changes in creatinine over the past 24 hours and hourly urine output are noted before surgery.
Assess whether diuresis is desired (e.g., to prevent ventricular failure, pulmonary edema) in oliguric or anuric patients.

Continuous Renal Replacement Therapy

The indications for continuous renal replacement therapy (CRRT) include ARF, fluid overload, severe sepsis, heart failure, and cerebral edema. These indications and the nature of the surgery guide the decision to provide CRRT in the operating room (OR).
CRRT can be safely discontinued for a short period of time for minor procedures with minimal fluid requirements or hemodynamic instability (e.g., tracheostomy, secondary wound closure).
Patients receiving CRRT are often hemodynamically unstable.
Adequate staffing and equipment are needed if CRRT is continued in the OR.
Many patients undergoing CRRT require anticoagulation to minimize filter and circuit clots, therefore close coordination with the surgeon and the physician managing the CRRT balances the risk of major bleeding with CRRT clotting (19).

ENDOCRINE/METABOLIC

Stress-induced hyperglycemia is commonly seen in the critically ill patient. Adrenaline, cortisol, and tumor necrosis factor (TNF) alpha cause hyperglycemia via gluconeogenesis, and interventions such as steroids and total parenteral nutrition (TPN) increase blood sugar. There is a high risk for adrenal insufficiency from a variety of etiologies. Systemic inflammation seen in sepsis and ARDS directly cause HPA dysfunction. Exogenous corticosteroids treat disease processes (e.g., COPD exacerbations, pneumonia, bacterial meningitis, cerebral edema, sepsis, and ARDS), and cause iatrogenic HPA suppression.

Glucose Control

Intensive glucose control (81 to 108 mg/dL) is associated with hypoglycemia.
A target glucose level <180 mg/dL is reasonable in critically ill patients.
The preoperative assessment evaluates insulin requirements in the ICU and anticipates monitoring and treating blood sugar levels in the OR (20).

Adrenal Insufficiency

The incidence of adrenal insufficiency ranges from 32% in postoperative surgical ICU patients to 61% in septic patients (21,22).
An AM cortisol <10 to 15 µg/dL suggests relative adrenal insufficiency (inadequate cortisol production in response to critical illness) (22).
Hydrocortisone (200 mg per day) may decrease vasopressor requirements in patients with relative adrenal insufficiency (12).

HEMATOLOGIC

Decreased red blood cell (RBC) lifespan, excessive blood sampling, and decreased production cause anemia in the ICU (23).

Assess the cause of anemia before surgery.
Hemolysis, oozing at injury sites, and gastrointestinal bleeding may be causative.
“Anemia of investigation” is iatrogenic anemia from diagnostic phlebotomy in the ICU, which can total 40 to 70 mL of blood loss daily, which exceeds the normal healthy replacement rate.
Nutritional deficiencies (vitamin B₁₂, folate, iron) and anemia of chronic disease cause decreased production of RBC.

GASTROINTESTINAL

Intra-Abdominal Hypertension and Abdominal Compartment Syndrome

Intra-abdominal hypertension (IAH) is defined as intra-abdominal pressures >12 mm Hg. Abdominal compartment syndrome can occur at any pressure though is typically associated with intra-abdominal pressures >20 mm Hg and requires IAH-induced organ dysfunction for diagnosis. The definitive diagnosis of abdominal compartment syndrome requires determination of intra-abdominal pressure, measured via intravesical (bladder) pressure.

IAH displaces the diaphragm cephalad, and decreases venous return and CO.
IAH causes elevated peak inspiratory and mean airway pressures, hypoxemia, hypercarbia, renal impairment, mesenteric ischemia, sepsis, and lactic acidosis.
Risk factors for IAH include abdominal surgery, massive fluid resuscitation, ileus, intra-abdominal infection, and sepsis.
IAH classically presents with a tense abdomen, but physical examination is a poor predictor of IAH.
Supportive therapy includes gastric and rectal decompression, lowering the head of bed, sedation, and neuromuscular blockade. Definitive management is laparotomy with surgical decompression (24).

NUTRITION

Prolonged fasting compromises wound healing, increases risk of infection, and prolongs ICU stays. During the acute phase of critical illness, nutrition is often interrupted and patients do not receive needed calories (25).

Permissive underfeeding (hypocaloric feeding) during the first week of critical illness has not been associated with worse outcomes compared to patients who receive early full feeding (26,27,28).
Reinitiating nutrition in patients who have had depletion of micronutrition stores can cause “refeeding syndrome” marked by severe hypokalemia and hypophosphatemia.
Patients may have delayed gastric emptying from ileus, impaired gut motility from vasopressor therapy, or diabetes mellitus.
Assessing gastric residual volumes from enteral nutrition is performed before airway management.
Fasting recommendations for intubated patients before surgery:
- Nonabdominal surgery: Stop gastric feeding 45 minutes before transport and flush and aspirate the gastric tube.
- Abdominal or airway surgery: Nil per os for 6 hours before planned anesthesia, and flush and aspirate the gastric tube.
- Postpyloric feeding: Feeds may be discontinued or continued before transport depending on local practice (29).

Total Parenteral Nutrition

The major risks of TPN in the OR include inadvertently changing the rate or interruption of TPN and contamination of the TPN access catheter. There are two common approaches to TPN in the OR:

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