CHAPTER 30 Intracranial Pressure and Neuromonitoring
Pavis Laengvejkal1 and Stephan A. Mayer2
1 Bumrungrad International Hospital, Bangkok, Thailand
2 New York Medical College, Valhalla, NY, USA
Intracranial pressure monitoring
Overview
ICP represents the pressure within the dura.
The normal value is 3–15 mmHg (or 5–20 cmH2O).
Increased ICP leads to cerebral ischemia and herniation and requires immediate treatment.
Monro–Kellie doctrine
The Monro–Kellie doctrine states that the cranial vault is a fixed space containing three volumes: blood, cerebrospinal fluid (CSF), and brain.
Any space‐occupying lesion or increased volume of intracranial constituents may lead to increased ICP.
Intracranial compliance
Intracranial compliance is defined as the change in volume over the change in pressure (dV/dP).
Compliance decreases as intracranial volume increases (Figure 30.1).
In the initial phases of an ICP‐elevating process, as volume is added to the skull (point A), CSF is displaced into the spinal thecal sac and blood is decompressed from the distensible cerebral veins.
If compensatory redistribution mechanisms are exhausted ICP can increase profoundly with small increments of additional volume (point B).
The amplitude of the ICP pulse wave may provide a clue that compliance is reduced; as compliance falls, the ICP pulse amplitude increases (point B, inset).
Cerebral perfusion pressure
Cerebral perfusion pressure (CPP) is calculated as mean arterial pressure (MAP) minus ICP.
A consequence of elevated ICP is lowering of cerebral blood flow (CBF) and secondary hypoxic–ischemic injury.
CPP determines CBF and should remain above 60 mmHg.
Autoregulation of the cerebral vasculature maintains CBF at a constant level of between 50 and 100 mmHg. Brain injury can impair autoregulation and cause CBF to approximate a more straight line relationship with CPP (Figure 30.2).
Pathologic pressure waves
In patients with raised ICP, pathologic ICP waveforms may occur (Figure 30.3).
Lundberg A waves (or plateau waves) represent prolonged periods of profoundly high ICP. They are ominous, and abruptly occur when either CPP or intracranial compliance is low. Their duration is from minutes to hours, and levels as high as 50–100 mmHg may be reached.
Lundberg B waves are of shorter duration and have lower amplitude elevations that indicate that intracranial compliance reserves are compromised.
Conditions associated with increased ICP
Clinical features of elevated ICP
Clinical manifestations of increased ICP are varied and unreliable.
Features include depressed level of consciousness, nausea and vomiting, headache, blurring of vision, and diplopia (from sixth nerve palsies).
Cushing’s triad may be observed: increased arterial blood pressure associated with bradycardia and irregular respirations.
Increased ICP can lead to herniation syndromes, which result from brain tissue shifting related to compartmentalized pressure gradients.
Herniation syndromes
Type
Clinical hallmark
Causes
Uncal (lateral
Ipsilateral CN3 palsy
Temporal lobe
transtentorial)
Contralateral or bilateral
mass lesion
motor posturing
Central transtentorial
Progression from
Diffuse cerebral
bilateral decorticate to
edema, hydrocephalus
decerebrate posturing
Rostral–caudal loss of brainstem
reflexes
Subfalcine
Asymmetric (contralateral >
Convexity (frontal or
ipsilateral) motor posturing
parietal) mass lesion
Preserved oculocephalic reflex
Cerebellar (upward
Sudden progression to coma
Cerebellar mass lesion
or downward)
with bilateral motor posturing
Cerebellar signs
Indications for ICP monitoring
Patients should generally meet three criteria prior to placement of an ICP monitor:
Brain imaging reveals a space‐occupying lesion or cisternal effacement suggesting that the patient is at risk for high ICP.
The patient is comatose (GCS score of ≤8).
The prognosis is such that aggressive ICU treatment is indicated.
ICP monitoring devices
Several types of ICP monitors exist.
The external ventricular drainage (EVD) catheter is the gold standard; it consists of a water‐filled catheter which is placed through a burr hole into the ventricle and connected to a pressure transducer set at head level.
EVD allows for both ICP monitoring and the ability to perform therapeutic CSF drainage.
A major drawback of EVD is the risk of infectious ventriculitis, which occurs in approximately 10–15% of patients and steadily increases until the 10th day of use.
The best alternatives to EVD include fiberoptic transducers (Integra®) or pressure microsensors (Codman®) placed through a burr hole either into the parenchyma or ventricle. These devices carry a minimal risk of infection and are highly reliable.
Treatment of ICP
There are two scenarios for ICP management:
Hyperacute situation during which brain herniation is taking place. Treatment is an all‐out approach to immediately protect the brainstem pending definitive surgical intervention or placement of an ICP monitor:
Elevate head of bed 30–45°.
Normal saline (0.9%) at 80–100 mL/h (avoid hypotonic fluids).
Intubate and hyperventilate (target PCO2 = 28–32 mmHg).
Mannitol 20% 1–1.5 g/kg via rapid IV infusion.
Foley catheter.
CT scan and immediate neurosurgical consultation.
Monitored patients in the ICU setting. This algorithm should be initiated any time ICP remains greater than 20 mmHg for more than 10 minutes:
Consider repeat CT scanning and surgical removal of an intracranial mass lesion, or ventricular drainage.
Intravenous sedation with fentanyl and propofol to attain a motionless, quiet state.
Reduction of blood pressure if CPP remains >110 mmHg, or vasopressor infusion if CPP <70 mmHg.
Mannitol 0.25–1 g/kg IV (repeat every 1–6 hours as needed).
Hyperventilation to PCO2 levels of 28–32 mmHg.
Paralysis with neuromuscular blockade.
High dose pentobarbital therapy (load 5–20 mg/kg and infuse 1–4 mg/kg/h).
Hypothermia with external cooling to 32–34°C.
Multimodality neuromonitoring
Brain oxygenation monitoring
The human brain consumes 20% of total body oxygen.
Approximately 90% of the energy is used by neurons, mainly for synaptic activity and to preserve ionic gradients. The energy substrate is high energy phosphate (ATP), produced from glucose through aerobic metabolism.
In the absence of continuous oxygen delivery, ATP production ceases within seconds. Osmotic gradients are lost, edema sets in, intracellular calcium rises, and early apoptotic mechanisms are triggered.
With new technology early detection and reversal of brain hypoxia is feasible. Two invasive bedside techniques allow for brain oxygenation monitoring: brain tissue oxygen partial pressure (PbtO2) and jugular venous oxygen saturation (SjvO2) monitoring.
Both SjvO2 and PbtO2 are dependent on CBF, arterial O2 content, and cerebral metabolic rate ofO2 consumption (CMRO2). AVDO2, the arteriovenous difference in O2 content, can be simplified as SaO2 – SjvO2, since other parameters, like hemoglobin, remain constant during cerebral transit.
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