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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_885_Библиотеки_им_академика_М_И_Перельмана.pdf
288 E. L. Jones, T. S. Jones and C. A. Porter
Background
• Rhabdomyolysis was originally described after crush injuries in World
War II; however, in the civilian setting it can also be seen with prolong immo bilization and illicit drug or alcohol use. Common examples of iatrogenic
immobilization leading to rhabdomyolysis include prolonged neuromuscular paralysis during critical illness and during bariatric surgery in
morbidly obese patients (Chapter 25).
• Rhabdomyolysis is diagnosed based upon history, physical exam and a serum
creatine kinase (CK) level greater than five times the upper limit of normal
(approximately 5000 IU/L).
• Up to 60% of patients with rhabdomyolysis will experience acute kidney
injury via three major mechanisms: (1) volume depletion (hemorrhage, dehydration and necrotic skeletal muscle that can sequester up to 12L of fluid);
(2) tubular obstruction by heme pigment deposition; and (3) direct tubular
injury from free iron.
• Rhabdomyolysis should be considered whenever a compartment syndrome
(especially in the lower extremity) is diagnosed. Alternatively, aggressive
fluid resuscitation while treating rhabdomyolysis from other etiology can create a compartment syndrome.
• The mainstay of treatment is preservation of renal function which requires
aggressive, isotonic fluid resuscitation for a goal urine output between 2–3 cc/
kg/hr (200–300 mL/h). Urine alkalinization, forced diuresis and other adjunctive treatments have not proven beneficial in large studies unless patient
presents evidence of acute kidney injury (Cr > 2.0 mg/dL).
Main Body
Pathology
• Skeletal muscle injury and necrosis results in the release of intracellular contents; including the compact heme-protein: myoglobin.
• Heme-proteins contain significant amounts of iron which is normally excreted
by kidneys. However, when intra-tubule concentrations rise, they can be
directly nephrotoxic and can also cause renal tubule obstruction. When combined with hypovolemia, significant renal injury can occur which often leads
to associated electrolyte abnormalities (most commonly hyperkalemia,
hypocalcemia and hyperphosphatemia).
• Rhabdomyolysis rarely occurs in isolation and the simultaneous management
of concomitant trauma and organ dysfunction must also be done.
Rhabdomyolysis 289
• High-risk populations include: morbidly obese, prolonged surgery, prolonged
seizure activity, traumatic crush injuries, statin use, and illicit drug use.
• Recurrent episodes may be a sign of a defect in muscle metabolism.
Diagnosis
•· History — rhabdomyolysis can often be diagnosed based upon history alone:
recent trauma or exertional activity, prolonged immobilization and illicit drug
or alcohol use are all possible causes of rhabdomyolysis.
{ Common myotoxic medications may also lead to significant rhabdo-
myolysis: HMG-CoA reductase inhibitors (especially when used with
nicotinic acid), cyclosporine, itraconazole, erythromycin, colchicine and
corticosteroids.
• Common signs and symptoms:
{ Pain, swelling, weakness or other signs of muscle injury (crush, elevated
compartment pressures, etc.).
{ Changes in urine: “tea-colored”
Myoglobin appears when it exceeds the renal threshold (>1.5 mg/dL
on urinalysis, serum > 100 mg/cL).
• Lab testing
{ Creatine kinase (CK), (normal <100 IU/L)
No known threshold for increased AKI risk.
Rhabdomyolysis confirmed by CK > 5000 IU/L.
Follow every 4–6 hours until CK level peaks.
{ Serum creatinine (Cr) — confirms renal injury but is non-specific.
{ Myoglobinuria — often used as a qualitative test to confirm risk for rhabdo-
myolysis but not routinely followed. Note: a urine dip that is positive for
heme in the absence of RBCs on urinalysis is indicative of myoglobinuria
(urine dip does not distinguish between hemoglobin and myoglobin).
• Muscle biopsy — not recommended (diagnoses muscle necrosis but this is
non-specific and does not change management).
Treatment
• Aggressive volume resuscitation to restore renal perfusion:
{ Dilutes nephrotoxins.
{ Restores renal tubule flow.
290 E. L. Jones, T. S. Jones and C. A. Porter
{ Treats concomitant hypovolemia which can be more injurious than the
direct toxic effect of heme-proteins.
{ Isotonic fluids are recommended: normal saline or lactated ringers (LR
has shown a small benefit over NS in patients with rhabdomyolysis secondary to doxylamine intoxication).
{ Goal: urine output 2–3 cc/kg/hr.
• Alkalinization of urine
{ Myoglobin precipitates in an acidic environment; therefore bicarbonate
use has theoretic benefit.
{ Treat to goal urine pH > 6.5.
{ Monitor arterial blood gases at least twice daily and be wary of both alka-
losis and hypernatremia.
{ Benefits of urine alkalinization have not been established in large trials
but should be considered in patients presenting with, or with a history of,
renal failure (Cr > 2.0 mg/dL).
• Mannitol (forced diuresis)
{ Theoretically increases urine flow and tubule flushing.
{ No randomized control trials: consider only in patients who are fluid
replete as hypovolemia will worsen renal injury.
• Treat concomitant electrolyte abnormalities: most commonly hyperkalemia,
hypocalcemia and hyperphosphatemia.
Rhabdomyolysis 291
h
5
Practical Algorithm(s)/Diagrams
Table 1. Common causes of rhabdomyolysis
Hypoxic/Trauma Exertional Chemical Genetic Defects Infections
Burns/
Electrocution
Compartment Disorders of lipid
Syndrome Extreme exertion Alcohol metabolism Epstein-Barr virus
Prolonged
Immobilization
Sickle cell trait Hyperthemia Derangement disorders
Trauma/Crush
Injury
Delirium Tremens Statins/
Fibrates
Disorders of
glycolysis/
Influenza A and B
glycogenolysis
Hypo/
Hyperthemia
Heroin/
Cocaine
Mitochondrial
Disorders
HIV
Malignant Electrolyte Purine nucleotide Legionella
Prolonged Seizure Pyomuositis
Status asthmaticus Clostridium
Snake venom/
spider bites
CK < 5000 IU/L
Repeat 4 hours
CK < 5000 IU/L
No rhabdomyolysis
H&P suspicious for muscle
necrosis
Draw serum CK + Cr
CK > 5000 IU/L
Cr < 2.0 mg/dL AND
No history of renal failure
LR or NS 2-3cc/kg/hr
Goal: 200-300mL/hr)
Q4H CK unƟl decreasing
IF UOP < 100mL/hr OR
Impending AKI
Aggressive fluid resuscitaƟon
1/2NS + 100meq HCO3 @ 125mL/
(Serial ABGs & DC if serum pH > 7.
For GOAL UOP > 100mL/hr x 12hr
Fig. 1. Rhabdomyolysis algorithm.
CK > 5000 IU/L
Cr > 2.0 mg/dL OR
History of renal failure
AND
AND
Mannitol 12.5g IV q6H
292 E. L. Jones, T. S. Jones and C. A. Porter
Review of Current Literature with References
Review article
• Zimmerman and Shen published a review of the literate in CHEST in 2013. In
particular, Tables 1 and 2 describe extensively the common causes and medications that are associated with rhabdomyolysis. They accurately describe the
common treatment recommendations and lack of Level 1 data to guide practitioners. Zimmerman JL, Shen MC, Rhabdomyolysis. CHEST 2013; 144(3):
1058–1065.
IVF resuscitation
• Cho et al. randomized 28 patients to LR vs NS resuscitation for doxylamine
succinate induced rhabdomyolysis. This anticholinergic drug is used for insomnia and is seen in 25% of drug overdose patients in Korea. There was no
difference in time to normalization of CK levels; however, patients resuscitated with NS did develop a metabolic acidosis and required more sodium
bicarbonate to achieve urine alkalinization. Patients treated with LR did not
develop signifi cant hyperkalemia. Cho YC, Lim H, Kim SH, Comparison of
lactated Ringer’s solution and 0.9% saline in the treatment of rhabdomyolysis
induced by doxylamine intoxication. Emerg Med J 2007; 24(4): 276–280.
Role of diuretics
• Brown et al. looked at 2083 trauma admissions who had CK levels >5000 U/L.
There was no difference in rates of renal failure, need for dialysis or mortality
in patients who received bicarbonate and mannitol prophylactically and those
who did not. Brow CV, Rhee P, Chan L, Evans K, Demetriades D, Velmahos
GC, Preventing renal failure in patients with rhabdomyolysis: do bicarbonate
and mannitol make a difference? J Trauma 2004; 56(6): 1191–1196.
8. Gastrointestinal
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Chapter 8-(i)
Nutrition in the Critically Ill
Michael A. Maccini, MD* and Ernest E. Moore, MD
†
Professor of Surgery and Vice-Chair of Surgical Research, University of Colorado
*Surgical Resident, University of Colorado School of Medicine
School of Medicine
Take Home Points
• Nutritional assessment, support, and monitoring are essential in the care of
the critically ill. Ongoing monitoring of the patient’s nutritional status and
appropriate adjustments to the nutritional regimen are essential.
• The physiologic stress of critical illness results in a complex hypercatabolic
state and metabolic derangements which must be taken into account when
estimating patients’ nutritional requirements.
• The goal of nutritional support is to maintain positive nitrogen balance to
attenuate loss of protein in the form of muscle mass.
• Generic nutrition goals should be 25 non-protein calories/kg per day and
2 g/kg protein per day, based on the patient’s adjusted feeding weight.
Further protein needs may result from additional external losses; e.g., open
wound, hemodialysis, ascitic or lymphatic leak.
†
Contact information: (Michael A. Maccini) 777 Bannock St, MC 0206, Denver, CO 80204;
(Ernest E. Moore) 655 Broadway, Ste. 365, Denver, CO 80203; Tel.: 303-602-1820, email:
Ernest.moore@dhha.org; Michael.Maccini@dhha.org
295
296 M. A. Maccini and E. E. Moore
• Enteral feeding should not be held for surgical procedures in mechanically
ventilated patients (airway is already secure).
• Enteral nutrition is superior to total parenteral nutrition and should be
initiated early in hospitalization.
• Total parenteral nutrition may be necessary if enteral nutrition is contraindicated, but is associated with an increased risk of complications. Patients on
TPN require close monitoring for evidence of complications.
• Hyperglycemia should be minimized by ongoing monitoring and corrected in
critically ill patients.
Background
• Patients with prolonged ICU stays are vulnerable to substantial protein
deficits. Measurable loss of muscle mass has been documented in ICU
patients within a few days. Weakness due to these deficits is associated with
prolonged mechanical ventilation, and immunosuppression which increases
the risk of infection.
• Critically ill patients have increased energy expenditures due to the hypermetabolic state resulting from underlying acute illness or injuries.
{ Levels of stress hormones (cortisol, epinephrine, norepinephrine,
glucagon, etc.) are elevated and increase systemic metabolic activity,
including gluconeogenesis.
{ In addition, increased levels of tissue necrosis factor (TNF), and other
cytokines such as IL-1 and IL-6 increase systemic inflammation and, thus
increases metabolic demands.
{ Growth hormone and insulin-like growth factor 1 (IGF-1) are anabolic
hormones whose levels are suppressed following injury, shifting the
overall metabolic balance to catabolism and increasing the body’s use of
amino acids for gluconeogenesis.
{ Finally, the central nervous system responds to afferent signals alerting it
to injury by stimulating sympathetic “fight or flight” responses, resulting
in further release of pro-inflammatory mediators and catecholamines via
activation of the hypothalamic-pituitary-adrenal axis.
• Malnutrition in the critically ill is due to abnormal processing of nutrients.
The objective of nutritional support in the ICU is to maintain muscle/protein
mass by minimizing catabolism, with the goal of preserving as much
functionality as possible. Without addressing the underlying injury and other
Nutrition in the Critically Ill 297
sources of inflammation, even adequate nutritional supplementation cannot
preserve lean body mass.
Main Body
• Nutritional Assessment
{ Accurate assessment of a patient’s nutritional status and needs requires a
history, physical exam, and interpretation of laboratory data.
History of present illness should include a list of the patient’s current
injuries with level of severity, which allows for estimation of the
patient’s level of physiologic stress. Medical and surgical histories
provide a picture of the patient’s baseline level of function, preexisting conditions — including weight loss and other signs of
malnutrition — and potential anatomic alterations that may affect
nutrition administration. Social history provides information
regarding a patient’s drug and alcohol use, as well as a support
network to aid in discharge planning once inpatient care is no longer
required.
Physical exam should include an estimation of the patient’s muscle
mass, caloric reserves, and fluid status. Body Mass Index (BMI) is an
important measure, as underweight and obesity are both forms of
malnutrition affecting nutritional needs and interventions.
Pertinent laboratory data may include albumin, prealbumin, transferrin,
LFTs, electrolyte levels, CBC, and ABGs.
Ö Albumin, prealbumin and transferrin are constitutive proteins
produced by the liver, and levels of production tend to drop in the
acute post-surgical period or after injury as synthesis switches to
production of acute phase proteins. Adequate nutritional support in
conjunction with treatment of acute illness facilitates stress
response resolution and inflammation reduction, and should
ultimately result in normal serum protein levels. Acute phase
protein monitoing, however, has limited clinical utility until
systemic inflammation has resolved. Interpretation of serum
protein levels may be less reliable in patients with underlying
liver dysfunction and resulting baseline serum protein level
derangements.