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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5524_Библиотеки_им_академика_М_И_Перельмана.pdf
278 D. Lollar
{ Each patient is only allowed one metabolic disturbance (either acidosis or
alklalosis) and one respiratory disturbance (either acidosis or alkalosis).
That is, a patient cannot have both a respiratory acidosis and respiratory
alkalosis at the same time. By contrast, a patient may have both a metabolic acidosis and respiratory alkalosis.
{ Anion gap is calculated as [Na] − ([Cl] + [HCO
]). A value of 9 ± 3 is
3
considered normal. The anion gap must be corrected for the albumin level
as every decrease of 1.0 (g/dL) from a normal albumin decreases the normal value for the anion gap by 2.5. Failure to do so will result in
misinterpretation of an anion gap acidosis as a non-anion gap acidosis in
the hypoalbumenemic patient. For example, a patient with an uncorrected
anion gap of 9 and a serum albumen concentration of 2.0 (UNITS) has a
corrected anion gap of 14.
{ The three most common causes of non-anion gap metabolic acidosis in
the surgical ICU are hyperchloremia, gastrointestinal loss of bicarbonate,
and renal tubular acidosis. Hyperchloremic metabolic acidosis results
from excessive administration of chloride-rich fluid, usually in the context
of resuscitation. Failure to recognize this etiology of acidosis may result
in misinterpretation, followed by additional administration of chloride
rich-fluid, exacerbating the acidosis. This may be avoided by always
checking the anion gap and serum chloride concentration in every critically ill patient with a metabolic acidosis.
{ Simple respiratory acidosis should be compensated with an elevated
bicarbonate level. In simple, acute respiratory acid-base disturbances, the
pH changes by 0.08 for each change in pCO2 of 10 mm Hg in the oppo-
site direction. For example, a patient with a pH of 7.32 and a pCO2 of
50 mm Hg has a simple respiratory acidosis. A pH < 7.32 in this situation
suggests a superimposed metabolic acidosis. By contrast, a pH > 7.32 in
this situation suggests a superimposed metabolic alkalosis (or chronic
compensation of the respiratory acidosis). Another helpful relationship is
that a normal compensation for an elevated pCO2 is 1 mmol/L increase
in bicarbonate for every 10 mmHg increase in pCO2. For example, a
patient with a pCO
of 60 mmHg should have a serum HCO
2
−
concentra-
3
tion of approximately 20 mmol/L.
{ Simple metabolic acidosis is initially compensated for by increasing venti-
lation and decreasing pCO2 levels to create a relative respiratory alkalosis;
however this compensation will never fully normalize the pH. The expected
change in pCO2 in the setting of a pure metabolic acidosis is expressed
using the Winter’s formula: expected pCO2 = 1.5(HCO
−
) + 8 ± 2. Thus, a
3
Electrolytes 279
patient with a pH of 7.30 and a HCO
−
of 10 would have an expected
3
pCO2 of 23 mmHg. An actual pCO2 < mmHg would suggest a secondary
respiratory alkalosis; whereas an actual pCO2 > 23 mmHg suggests a
superimposed respiratory alkalosis.
{ Treatment of a metabolic acidosis involves treatment of the underlying
cause. Typically this involves aggressive crystalloid resuscitation and
disease specific interventions, e.g insulin administration for diabetic
ketoacidosis, dialysis for severe uremia, etc.
{ Respiratory acidosis up to a pH of 7.15 may be safely tolerated in order
to manage plateau airway pressures in patients with Acute Respiratory
Distress Syndrome and impaired ventilation. This strategy is termed permissive hypercapnea [chapter 5-(v)]. A pH below 7.15 should be managed
with bicarbonate administration (typically sodium bicarbonate infusion)
and vasopressors for cardiac instability.
• Alkalosis
{ Alkalosis is identified by an elevated pH (>7.40). A lowered pCO
the setting of a pH > 7.40 indicates a respiratory etiology while an
elevated bicarbonate concentration in the setting of a pH > 7.40
indicates a metabolic cause.
{ An elevated bicarbonate level can be caused by: (1) loss of hydrogen ions;
(2) a gain of bicarbonate ions; or (3) a decrease in extracellular volume
(contraction alkalosis). Metabolic alkaloses are typically asymptomatic
though can be associated with other electrolyte abnormalities which may
produce symptoms.
{ The three most common causes of metabolic alkalosis in the surgical ICU
are hypokalemia, gastrointestinal loss of acid, and volume contraction as
a result of diuretic therapy.
{ Initial evaluation of a metabolic alkalosis involves investigating the urine
chloride level. In chloride-responsive alkaloses, a chloride deficient state
(typically due to volume contraction secondary to diuretics, nasogastric
tube suction or laxative abuse) impairs the resorption of bicarbonate in the
distal collecting ducts.
{ Chloride responsive alkalosis is best treated with fluid resuscitation
with chloride-containing IVF (e.g normal saline.) To estimate chloride
need, a chloride deficit is calculated by the formula 0.2 × weight (kg) ×
(100−[Cl]). The fluid required to meet this deficit is then calculated by the
chloride deficit divided by the mEq/L of chloride in the fluid being
administered (154 mEq/L in normal saline).
in
2
280 D. Lollar
{ Patients with an elevated urine chloride (>40 mEq/L) have a “chloride
resistant” alkalosis due to primary or secondary mineralocorticoid excess.
This is typically associated with increased extracellular volume.
{ Chloride-resistant alkalosis management should initially begin with
correction of associated hypokalemia. The carbonic anhydrase inhibitor
acetazolamide is typically sufficient management if potassium replacement is insufficient. Very rarely, a dilute hydrochloric acid infusion is
required to correct severe, refractory alkaloses.
{ The excess HCO
accumulated as a result of a metabolic alklalosis may
3
serve as a helpful buffer to prevent the rapid development of a respiratory
acidosis in a patient with deteriorating ventilation. For this reason, we do not
routinely correct mild to moderation metabolic alkalosis (pH 7.40 – 7.60).
• Derangements of plasma sodium
{ Hyponatremia is the most common electrolyte abnormality in the surgical
ICU and is caused by a relative increase in body water compared to plasma
sodium concentration. Premenopausal women, children and hypoxic
patients are most at risk for developing life-threatening hyponatremic
encephalopathy despite sodium levels that may not be severely deranged.
{ Evaluation of hyponatremia begins by ruling out pseudohyponatremia: pseu-
dohyponatremia exists when the absolute amount of sodium in the serum is
unchanged, but there is an excess of water secondary to another osmotically
active substance. The most common examples are glucose (hypergylcemia)
and mannitol. In this case, the serum osmolarity will be normal. An approximate correction factor for hypergylcemia is that, for every increase in the
serum glocuse level above 100 g/dL, 2.5 meQ/L can be addded to the serum
sodium concentration. For example, the corrected serum sodium concentration for a patient with a serum sodium concentration of 130 mEq/L and a
serum glucose concentration of 500 g/dL would be 140 mEq/L.
{ After pseudohyponatremia is ruled out, the urine osmolarity is checked;
urine osmolairty < 100 mOsm/kg in the setting of hyponatremia is due to
iatrogenic administration of hypotonic fluids in the surgical ICU patient
(the most common cause of hyponatremia) or psychogenic polydipsia in
the outpatient.
{ In patients with a low serum osmolality and normal to elevated urine osmo-
lality, a combination of the total body volume status and urinary sodium
concentration will categorize the remaining causes of hyponatremia.
Hypervolemia indicates underlying organ dysfunction (congestive
heart failure, cirrhosis or renal failure) as the causal problem.
Electrolytes 281
Euvolemic patients with a normal urine sodium (>25 mOsm/kg) have
SIADH which can be caused by multiple etiologies including nausea,
postoperative state, pain, or stress.
Hypovolemic patients with a low urine sodium (< 25 mOsm/kg) are
dehydrated. In this case, the need to maintain volume status trumps
the need to maintain eunatremia, and water is reabsorbed in response
to increased ADH activity.
Hypovolemia with a normal to high urine sodium (> 25 mOsm/kg) is
most commonly seen with cerebral salt wasting, a poorly understood
sequellae of traumatic brain injury in which urinary reabsorption of
sodium is impaired. Mineralocorticoid deficiency is another less
common cause of hypovolemic hyponatremia.
{ Symptoms of hyponatremia including seizures and respiratory arrest
should be treated with a NaCl 3% bolus of 100 mL over 10 minutes. This
can be repeated up to two times if necessary. In patients with severe symptoms such as prior seizure, lethargy, headache or nausea and vomiting or
those treated with a bolus should be started on a NaCl 3% infusion at
1 mL/kg/hr. Asymptomatic patients should be treated with fluid unless felt
to be hypovolemic. See Fig. 2.
{ Hypernatremia is precipitated by excess free water losses in patients with
impaired thirst mechanism or impaired water access. Common causes of
hypernatremia include diuresis due to medications or hyperglycemia,
gastrointestinal losses due to nasogastric suction or diarrhea, and insensible losses from the respiratory tract. Treatment consists of fluid
resuscitation with either lactated ringers or half normal saline for serum
sodium > 150 mEq/L. Free water needs are calculated by the free water
deficit: 0.6 × weight (kg) × ([Na] − 140)/ 140. Correction should be
gradual and should not exceed 1 mOsm/L/hr.
{ In patients with hypernatremia, central diabetes insipidus should be ruled
out as an underlying cause. This disease process is typically seen in
patients with cerebral pathology including traumatic brain injury, pituitary
surgery, and hemorrhagic stroke. The classic triad seen in diabetes insipidus is: (1) hypernatremia; (2) low urine osmolarity (<150 mOsm); and
(3) polyuria. Treatment consists of DDAVP administration.
• Derangements of plasma potassium
{ Potassium is predominantly intracellular and plasma levels represent only
a small level of total body potassium. Due to the curvilinear relationship
between plasma and total body potassium, twice as much total body
282 D. Lollar
potassium must be lost to decrease serum potassium levels for an equivalent increase in serum potassium versus increase in total body potassium.
{ Serum potassium levels below 3.5 mEq/L can be due to acute shifting of
potassium into cells thus decreasing plasma levels, or it may represent a
true decrease in total body potassium due to renal or extrinsic causes.
{ Transcellular movement of potassium into cells is precipitated by alkalo-
sis, insulin, β2 agonists, and hypothermia. These agents are used to treat
symptomatic or severe hyperkalemia. Treatment for transcellular hypokalemia involves treating the predisposing condition. Treatment for total
body potassium depletion is potassium repletion typically with KCl
though potassium phosphate is typically used for patients in diabetic
ketoacidosis. It is important to ensure adequate magnesium stores before
potassium repletion as hypomagnesemia prohibits effective repletion of
potassium.
{ Hyperkalemia is a much more dangerous condition than hypokalemia as
it can precipitate cardiac arrhythmias. Before pursuing aggressive therapy,
pseudohyperkalemia due to cell lysis in the blood sample must be
excluded as it occurs in up to 20% of samples. When an unexpected, precipitous change in potassium is found, a repeat sample should be sent to
confirm the finding.
{ In contradistinction to transcellular hypokalemia, causes of potassium
egress from cells include acidosis, β-blockers, medications (digitalis and
succinylcholine) and insulin deficient states.
{ Total body accumulation of potassium is due to failure to excrete potas-
sium in the urine, typically as a result of impaired renal function. Adrenal
insufficiency also causes impaired potassium excretion but hyperkalemia
is only seen in chronic disease. Definitive removal of potassium involves
potassium binding in the gut (kayexalate) and direct removal from the
blood through hemodialysis.
• Derangements of divalent ions
{ Magnesium deficiency is common in patients taking diuretics, having
diarrhea, with diabetes mellitus and in chronic alcoholics. Hypomagnesemia
can exacerbate cardiac irritability as it is “the body’s calcium channel
blocker.” Magnesium should be replaced in IV form as it is poorly
absorbed by the gut and precipitates diarrhea. Magnesium should be
replaced in hypokalemic patients.
Electrolytes 283
{ Hypermagnesemia is uncommon but can be seen in renal failure and mas-
sive hemolysis. Levels above 5 mEq/L can affect cardiac conduction
causing heart block and ventricular arrhythmias and should be treated
with IV calcium and hemodialysis.
{ Calcium is the most abundant electrolyte in the body but 99% is stored in
bone. Half of plasma calcium is bound to proteins and therefore inert.
Hypocalcemia may thus be due to low calcium levels or low protein (albumin) levels. Ionized hypocalcemia can be seen in sepsis, pancreatitis,
renal failure, alkalosis and concomitant with blood transfusions. Calcium
should be repleted orally or IV if severe. Calcium chloride is most effective for repletion but should only be used in emergency situations via a
central venous catheter.
{ Hypercalcemia is most commonly caused by cancer or hyperparathy-
roidism in non-ICU patients. Calcium levels above 12 mEq/L (or ionized
calcium >3.0 mmol/L) or in symptomatic patients (altered mental status,
EKG changes such as shortened QT interval) should be treated with volume expansion with normal saline and urinary calcium excretion with
loop diuretics such as furosemide.
{ Inorganic phosphate (PO
) resides predominantly intracellularly and par-
4
ticipates in glycolysis and ATP production. Dangerous hypophosphatemia
can be seen in malnourished patients who receive abundant glucose
administration. The movement of glucose into cells is accompanied by
phosphate, thus leading to dangerously low plasma phosphate levels if
total body phosphate is marginal. Treatment of this “refeeding syndrome”
is aggressive phosphate repletion and gradual advancement of glucose
administration (PO or IV) to goal in high-risk patients.
284 D. Lollar
Practical Algorithm(s)/Diagrams
Condition Expected Compensation/ Converison
Metabolic Acidosis 1 mmol/L HCO3 = 1 mmHg pCO
(Winter’s formula) pCO2 = 1.5 [HCO3] + 8 ± 2
pCO2last two digits of pH
Metabolic Alkalosis 1 mmol/L HCO3 = 0.7 mmHg pCO
Respiratory Acidosis (acute) 10 mmHg pCO
Respiratory Acidosis (chronic) 10 mmHg pCO2 = 4 mmol/L HCO
Respiratory Alkalosis (acute) 10 mmHg pCO2 = 2 mmol/L HCO
Respiratory Alkalosis (chronic) 10 mmHg pCO
Fig. 1. Work-up of acid/base derangements.
= 1 mmol/L HCO
2
= 4 mmol/L HCO
2
2
2
3
3
3
3
Fig. 2. Algorithm for evaluation of hyponatremia. UNa = urine sodium level.
Electrolytes 285
Review of Literature
• In an observational cohort study, 209 patients were categorized based on the
difference between prehospital anion gap and anion gap at ICU admission
(ΔAG) by 5 point intervals. Logistic regression compared ΔAG with all cause
mortality at 30, 90 and 365 days. A ΔAG of 5–10 correlated with an increased
odds ratio of 30 morality of 1.56 while a ΔAG of >10 correlated with an increased odds of death of 2.18. These results indicate that an increase in anon
gap of greater than 5 from prehospital to ICU admission predict the risk of all
cause mortality in the critically ill.
Lipnick MS, Braun AB, Cheung JT et al., Crit Care Med 2013; 41: 49–59.
• In a retrospective review of 300 critically ill ICU patients, base excess due to
unmeasured anions and anion gap were compared in their ability to predict
lactate levels. Logistic regression analysis showed a high degree of predictive
ability in all three variables to predict a lactate level > 5 mmol/L. Confi dence
intervals were 0.78–0.94 for base excess, 0.78–0.93 for base excess due to unmeasured anions and 0.77–0.92 for anion gaps. However, when compared to
the APACHE II score, none of these variables accurately predicted mortality.
Rocktaeschel J, Morimatsu H, Uchino S et al., Crit Care Med 2003; 31: 2131–2136.
• In 2012, the relationship between pre-intensive care unit potassium levels
were evaluated to see if an elevated potassium predicted mortality. Over
39,000 critically ill patients were evaluated in an observational study over
a ten-year period. Patients were grouped into cohorts based on peak potassium levels the day of ICU admission. Logistic regression analysis examined mortality at multiple time points. The odds ratio for increased mortality was statistically signifi cant at potassium levels greater than 4.5 but were
highest for patients with a highest potassium level greater than 6.5 mEq/L
(OR 1.72.) These data suggest that even modest elevations in a patient’s potassium level at ICU admission is associated with increased mortality.
McMahon GM, Mendu ML, Gibbons FK, Christopher KB, Intensive Care
Med 2012; 38: 1834–1842
• To determine if potassium repletion via continuous infusion was safe, 139
patients were enrolled in a randomized, open-label study comparing potassium
repletion with a continuous infusion versus the typical bolus administration
was performed in critically ill patients with serum potassium levels between
2.5 and 3.8 mmol/L. The primary outcome measured was the average difference in serum potassium levels over time. While the average serum potassium
was statistically signifi cant between the two groups by 0.22 mmol/L, this
286 D. Lollar
did not pre-determine level of treatment effect, calculated as 0.50 mmol/L.
However, there were no adverse effects noted due to the continual infusion of
potassium. This study suggests that repletion of mild to moderate hypokalemia can be safely and more effectively performed with a continuous infusion
versus a standard bolus repletion practice.
Chalwin RP, Moran JL, Peake SL et al., Anesthesia Intensive Care 2012; 40:
433–441.
Rhabdomyolysis
Chapter 7-(v)
Edward L. Jones, MD* Teresa S. Jones, MD†
and Clifford A. Porter, MD
*Surgical Resident, University of Colorado School of Medicine
†
Surgical Resident, University of Colorado School of Medicine
‡
Assistant Professor of Surgery, University of Colorado School of Medicine
‡
Take Home Points
• Rhabdomyolysis is injury of the skeletal muscle causing the release of
intracellular components that can overwhelm elimination mechanisms.
Myoglobinuria, electrolyte abnormalities and acute kidney injury (AKI) ensue.
• A high index of suspicion is required as rhabdomyolysis has numerous
causes and often requires concomitant management of multisystem trauma
(Table 1).
• The mainstay of treatment remains early and aggressive isotonic fluid resus-
citation for a goal urine output between 2–3 cc/kg/hr to minimize renal
injury.
Contact information: (Edward L. Jones and Teresa S. Jones) 12631 East 17th Ave, C313,
Aurora CO 80045; (Clifford A. Porter) Denver Veterans Affairs Medical Center, Eastern
Colorado Health Care System, 1055 Clermont St., Denver, CO 80220; Tel.: 303-399-8020,
email: Clifford.Porter3@VA.gov; Teresa.jones@ucdenver.edu; edward.jones@ucdenver.edu
287