Homeostatic Mechanisms in

the Neurosurgical Intensive

Care Unit Patient
Jerry Noel, Dan E. Miulli, Gayatri Santi, and Javed Siddiqi
Homeostasis of the Brain
The Monro-Kellie hypothesis states the skull is a solid box within which
the volume of all the components-the brain, cerebrospinal fluid (CSF),
and blood­should remain constant.

Alteration in pressure in one compartment of theis compensated by

volume changes in the other.
Cerebral Blood Flow and Perfusion
• Cerebral blood flow (50-75mL/100g/min) is affected by regional
cerebral metabolism, CPP, and oxygen and carbondioxide tension.
• Cerebral perfusion is the blood pressure gradient across the cerebral
vascula­ture and usually is equal to the mean arterial pressure minus
the intracranial pressure (MAP - ICP).
• One of the main objectives of the neurointensivists is to prevent
ischemia.
Control of Blood Pressure
• Significant decreases in blood pressure are a direct effect of ICP
treatments using sedation, paralytics, or diuretics. In these
hypotensive situa­tions, moderate intravenous (IV) fluids followed by
vasopressors can elevate blood pressure.
• In brain injury, the autoregulation of cerebral blood flow is altered; if
CPP increases above 95 to 1 25 mm Hg, there can be an increase in
blood volume and an increase in ICP. The first-line antihypertensive
medica­tion should be beta blockers or angiotensin-converting enzyme
(ACE) inhibi­tors.
Control of Serum Glucose
• Many authors express concern that even slightly elevated blood
glucose lev­els can cause or exacerbate secondary brain injury.
• Hypoglycemia of 50mg/dL causes neuronal injury by changing
cerebral blood flow and cerebral metabolism. In addition, glucose
levels > 110 to 150 mg/dL in nondiabetics and > 200 to 250 mg/dL in
diabetics also have dele­terious effects. Regular IV insulin infusion and
frequent blood glucose checks
areessentialtomaintainglucoselevelsbetween80and 110mg/dL.
• it is recommended to maintain blood glucose below 150 mg/dL.
Fluids and Electrolyte Balance
The principles of homeostasis of body water are as follows: two-thirds
of total fluid resides inside cells, and one-third of total fluid resides in
the extracellular space.

An estimate of serum osmolality is deter­mined by the equation

(2(Na+K)) + (BUN/2.8) + (Glucose/18)
Hypernatremia
• Hypernatremia is usually caused by hypovolemia due
to free water loss. It is often related to defective
antidiuretic hormone (ADH) release or due to osmotic
diuresis. When sodium levels are > 160 mmol/L,
decreased level of conscious­ness and confusion set in
• Hypernatremia should be treated first with crystal­
loids, 0.45 or 0.9% NaCI; if needed, colloids such as
5% albumin can be used
• Patients with diabetes insipidus should be carefully
monitored for fluid bal­ ance, body weight, serum and
urine sodium, and urine specific gravity. If urine
output exceeds the input by 250mL/h for 2
consecutive hours, hormonal replacement with IV 1-
deamino-8-D-arginine vasopressin (DDAVP, or desmo­
pressin) 0.5 to 2 J.lg may be administered with caution
Hyponatremia
• Hyponatremia should further be investigated and treated
when the serum sodium level is less than 131 mmol/L.
• In NICU patients, hyponatremia results primarily from SIADH
and CSW. In SIADH, the extracellular volume is increased, and
CSW is decreased.
• Patients usually become symptomatic after a drop of sodium
below 120 mOsm/L, although mentation changes can be
seen with levels below 130 mmoi/L in the acutely injured
patient. Some of the com­mon symptoms are headache,
nausea, and vomiting.
• The practitioner must distinguish the two disorders because
the main treat­ment for SIADH is fluid restriction. Urea,
diuretics, demeclocycline, and lithium may also be used.
• For CSW fluid and sodium chloride administration are the
principal therapies. Fludrocortisone may be considered in
subarachnoid hem­orrhage patients at risk of vasospasm, and
hydrocortisone may be used to pre­vent natriuresis
Hypothermia and Brain Injury
• Hypothermia is a great neuroprotectant and has consistently shown
benefit against a variety of brain injuries at the experimental level. It has
recently been shown to improve neurological outcome in comatose
survivors of cardiac arrest and neonatal hypoxia ischemia and is being
increasingly used by many centers for these conditions
• Brain temperature is higher than the core body temperature by 1oC.
Several studies demonstrate that in head-injured patients, there are
moderate to severe elevations in brain temperature. Hyperthermia is
neurotoxic, and hypo­thermia attenuates these effects.
• Mild hypothermia is defined to range between 32 and 35°C, and
moderate hypothermia, 30 and 33T