Page 1609 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

1128 PART 10: The Surgical Patient

phase response.” SIADH in this case may be due to the release of stored perfusion and oxygen delivery to the brain to prevent further secondary
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arginine vasopressin (AVP) from damaged neurons followed by a lack injury and hypotensive anemia should be treated with blood transfu-
of AVP if insufficient functional neurons remain. Therefore, periodic sions while the source of bleeding is determined and controlled. There
reassessment for SIADH and DI is wise. Both DI and SIADH usually is no evidence to define a particular target hemoglobin, platelet trans-
occur acutely within the first week post-TBI and SIADH usually resolves fusion, or INR threshold after general trauma, including after TBI. An
within 6 months, but rarely DI may persist. 48 analysis of the transfusion requirements in critical care (TRICC) trial
The most common etiology of hyponatremia post-TBI is SIADH, subset of multitrauma patients suggests that a restrictive transfusion
which accounts for 80% of cases. Brain tissue injury, elevated ICP, extra- target of Hb 7 g/dL is not inferior to a liberal target Hb of 10 g/dL.
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cranial trauma, and surgery are factors that may lead to inappropriately However, the transfusion threshold after TBI remains controversial.
elevated AVP. Another proposed mechanism for post-TBI hyponatremia A retrospective review of patients with severe (GCS <8) isolated TBI
is termed cerebral salt wasting (CSW) or renal salt wasting, caused by concluded that a restrictive transfusion practice (blood transfusion
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natriuretic peptide release from injured brain tissue leading to natriure- trigger Hb <8 g/dL vs Hb 8-10 g/dL range) is safe. A recent retrospec-
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sis and hypovolemia. ACTH deficiency occurs acutely in about 15% of tive review of 139 patients who were admitted with TBI and moder-
patients post-TBI; however, hyponatremia is only rarely due to glucocor- ate anemia (hematocrit 21-30) found no association between blood
ticoid deficiency. 51 transfusion and mortality, but blood transfusions and the transfusion
The differentiation between SIADH and CSW is not straightforward. volume were associated with poorer long-term functional outcomes.
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There is a complete overlap in laboratory parameters (including urine The authors concluded that transfusion should be aimed at patients
sodium and osmolality) with both conditions resulting in hyponatremia with symptomatic anemia or physiological compromise. Another
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and natriuresis. The diagnosis hinges upon an accurate assessment of study hypothesized that blood transfusions resulting in hematocrit
volume status; however, the traditional reliance on CVP leads to frequent values >28% at the end of the initial operating room phase would result
errors in intravascular volume assessment. Although controversy exists in more complications, increased mortality, and impaired recovery in
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about the existence of CSW and it may be relatively rare compared to severe TBI patients, 139 TBI cases were retrospectively reviewed and
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SIADH, euvolemia is consistent with SIADH and is treated with fluid blood transfusion resulting in hematocrit values >28% was not associ-
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restriction while hypovolemia is consistent with CSW that responds to ated with improved or worsened outcome.
saline hydration. There is a risk if fluid restriction is applied to the TBI Coagulopathy after general trauma is not well studied. Traumatic
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patient with CSW as this can exacerbate hypovolemia and potentially coagulopathy can be explained at least in part by tissue factor release
compromise cerebral perfusion. In the TBI patient with hyponatremia, into the general circulation with activation of the coagulation cascade
it is important to assess the serial changes in body weight and cumula- in both TBI and non-TBI. After TBI, abnormalities in coagulation
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tive fluid balance up to that point coupled with a reliable evaluation of include disseminated intravascular coagulation (DIC) (triggered by
hemodynamics (ie, not relying on CVP measurements—see previous systemic inflammation and tissue thromboplastin release or with multi-
section “Hemodynamic Monitoring and Management”). system trauma consumptive coagulopathy due to bleeding), thrombocy-
Both continuous maintenance fluids and fluid boluses for resusci- topenia, elevated INR, PTT, and hypofibrinogenemia. DIC occurs in 8%
tation should be provided with the goal of maintaining a euvolemic to 76% of patients after TBI depending on the definition of DIC and the
state while avoiding hypovolemia. Both hyper- and hypovolemia are severity of TBI. Consumptive coagulopathy due to bleeding requires
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associated with worse outcomes after TBI. Isotonic fluids that help surgical control of the bleeding source. Fresh frozen plasma with target
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to maintain the intravascular volume and not exacerbate cerebral INR below 2.0 and platelet transfusions to keep the levels at or above
edema or the tendency toward hyponatremia, such as normal saline 50,000/mm in the acute phase, if there is active bleeding or intracranial
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are employed for both continuous maintenance and bolus resuscita- hematomas, is common. Hypofibrinogenemia with fibrinogen levels
tion. If hyperchloremic metabolic acidosis occurs, a balanced isotonic <100 mg/dL is treated with cryoprecipitate.
fluid with buffer capacity (eg, acetate) such as Plasmalyte may be used. Intracranial bleeding is common after TBI and can worsen or be
Plasmalyte also contains magnesium and potassium which is convenient delayed. Hemostatic drugs may decrease the incidence or size of intra-
since hypomagnesemia and hypokalemia are common after severe TBI cranial bleeds; however, a recent review concluded that there is no
as is hypophosphatemia and all of these electrolytes frequently require reliable evidence from randomized controlled trials that hemostatic
supplementation. Although hypotonic fluids such as ½ normal saline drugs (aprotinin, tranexamic acid, aminocaproic acid, or recombined
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or 5% dextrose in water are usually avoided, they may be indicated if activated factor VIIa [rFVIIa]) reduce mortality or disability after TBI.
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there is significant hypernatremia, for example, >155 mEq/L. Severe Well-designed trials will be needed to assess the utility of these agents
hypo- or hypernatremia should be corrected gradually to avoid rapid after TBI.
fluid shifts across the blood brain barrier than can result in central pon-
tine myelinolysis or cerebral edema. ■ ANTISEIZURE PROPHYLAXIS
We have instituted the use of a continuous 3% saline infusion in There is a wide variability in the reported incidence of early (within 7
moderate and severe acute TBI patients upon admission in order to days; 4%-25%) versus late (>1 week; 9%-42%) posttraumatic seizures
prevent potentially harmful and commonly seen posttraumatic hypona- (PTS) in untreated patients. The incidence of seizures following pene-
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tremia that can cause significant brain swelling. The therapeutic goal is trating TBI is about 50% in patients followed for 15 years. 62,63 Risk factors
maintenance of serum sodium levels at 140 to 145 mEq/L. Although the for seizures after TBI include penetrating injuries, cortical contusion,
effect on outcome after TBI has not yet been determined, it does appear to depressed skull fractures, intracranial hematomas (epidural, subdural,
be successful in avoiding severe hyponatremia while helping to maintain intracerebral), seizures within the first 24 hours of injury, GCS <9, and
intravascular volume regardless of the etiology—SIADH or CSW (see also associated medical problems. 63-65 Seizures early after TBI may be associ-
“Hypertonic Saline” in “Treatment of Intracranial Hypertension”). ated with conditions that can result in further secondary brain injury
such as hypoxemia, hypercarbia, hypertension, increased ICP, increased
BLEEDING AND TRANSFUSION ISSUES cerebral metabolic rate, and excess release of toxic neurotransmitters.
Antiepileptic drugs are associated with adverse side effects including
Acute blood loss anemia is never primarily caused by closed space intra- skin rash, drug fever, elevated liver function tests, hematologic abnor-
cranial bleeding since death from herniation would occur far sooner malities, ataxia, and neurobehavioral side effects.
than anemia. Acute blood loss anemia, decreased red cell production, A large randomized, double-blind, placebo-controlled trial demon-
and coagulopathies occur as the result of traumatic injuries dictated by strated that phenytoin prophylaxis results in a significant decrease in
the degree of multisystem trauma. The concern after TBI is maintaining the incidence of early PTS (14.2%-3.6%) but no significant reduction

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