Prevent Increase in ICP
For acute patients with/at risk for raised intracranial pressure,
nursing care is provided that prevents elevations in ICP and/or
promotes ICP reduction including:
- Maintain good head and neck alignment
- Insert oral gastric drainage tube to maintain gastric decompression
(nasal tubes contraindicated)
- Maintain HOB elevation at 30 degrees
- Avoid hip flexion > 30 degrees (consider reverse trendelburg)
- Avoid positions that may increase abdominal or intrathoracic
pressures such as prone or semi-prone
- Minimize stimulation and lighting; space nursing care out to
avoid prolonged periods of stimulation
- Use sedatives/narcotics as ordered to minimize cough/gag; suction
only when needed
- If sedatives/narcotics fail to control cough in patients with
severe brain injury, review with physician other options such
as neuromuscular blockade.
- NMBs may help to reduce fever, but can also cause rapid lowering of body temperature. Hourly temperature monitoroing is required.
Note: if neuromuscular blocking agents are used to control ICP, Continuous EEG monitoring should be implemented as NMBs can mask seizure activity.
Implement Standards of Care for a Patient receiving Neuromuscular Blockade
Increased blood, CSF or tissue volume produces elevations in ICP.
Increased intrathoracic or intraabdominal pressures can increase
ICP. Nursing care goals include strategies that decrease/prevent
intrathoracic and intrabdominal pressure elevations, decrease metabolic
Although evidence is limited, HOB elevation to 30 degrees promotes
jugular venous drainage (to reduce cerebral blood volume). Higher
elevations may increase abdominal pressures or impede cerebral blood
Good head and neck alignment maintains jugular venous drainage.
Jugular venous drainage promote outflow of blood and CSF from the
In severely injured patients, drug induced coma may be used to
reduce brain metabolism. Propofol is the sedative of choice due
to the ability to rapidly awaken patient. It may also provide anticonvulsant
activities or offer some brain protection (unclear mechanism). Propofol
does not have analgesic properites. In mutiple trauma, anaglesia
should be administered with propofol.
Monitor Patient with Increased
For acute patients with/at risk for raised intracranial pressure,
additional monitoring is required as follows (report changes promptly to physician):
- Monitor core Temperature q 1 h. Continuous monitoring should
be considered if cooling blankets and/or neuromuscular blockers
are in use.
- Obtain order for acetaminophen and cooling blanket for T >
38. If fever is severe, review with physician other strategies
such as sedation or neuromuscular blockade.
- Lower temperature of cooling blanket gradually to avoid shivering.
- Wrapping arms and legs in blankets may reduce shivering.
- Neuromuscular blockers may help to reduced temperature and block shivering, but may cause rapid drop in temperature.
- Monitor BP and HR carefully. Treat hypotension and hypovolemia
- Maintain euvolemia.
- Monitor blood gases q 6 h and prn during acute phase. Keep PaCO2
35-40 (or lower if ordered) and PaO2 > 80-90
unless otherwise ordered. Unlike other ventilated patients, PaCO2 is the target, not the pH.
- If mannitol is ordered or hypertonic saline is used, measure serum electrolytes and osmolalities q 6
h as ordered. Notify Neurosurgeon if serum osmolality >320 (mannitol) or hypertonic saline (>340), of if serum sodium is > 156 with hypertonic saline.
- Monitor for increased/dilute urine output. Obtain order for serum and urine electrolytes and osmolality to assess for Diabetes Insipidus.
- Correct hyper/hyponatremia slowly (.5-1
mmol/L/hr of change in either direction (unless neurological death has been diagnosed and organ donation is being pursued).
- Monitor carefully for signs of seizure activity.
- Monitor blood sugar closely. Avoid hyper or hypoglycemia. Review target glucose with physician if insulin is required for an increase in the lower limit range.
- Monitor for seizure activity. Prophylactic anticonvulsants may be ordered for patients with injuries most likely to cause seizures.
Hypothalamus dysfunction can cause neurogenic fever and/or Diabetes
Insipidus (DI). Fever is associated with a poor neurological outcome
and increases the brains oxygen consumption. Shivering increases
metabolic rate and heat production, and promotes vasoconstriction
that reduces heat loss. Sedation and Neuromuscular Blockade can
lower temperature by decreasing heat production (due to muscle activity).
DI is diagnosed by presence of polyuria, low urine osmolality,
high serum osmolality and hypernatremia. It can cause severe and
lethal dehydration. Acute DI following severe brain injury is associated
with very poor outcome.
Hypercarbia, acidosis, hypoxemia or hypotension can trigger a sympathetic
rise in cerebral blood flow. Increased cerebral blood volume can
increase ICP. Patient triggered hyperventilation may be a sign of
Hypotension and/or hypovolemia can decrease cerebral blood flow.
A rise in BP may be a sign of increased ICP as the body attempts
to maintain cerebral perfusion pressure (CPP). Hypertension with
widening pulse pressure (increased systolic and decreased diastolic
pressure), bradycardia and irregular respirations or apnea suggestions
brainstem herniation (Cushings Triad). Urgent intervention is needed.
Hyponatremia can induce seizures (critical threshold <120 mmol/L;
critical level may be higher in patient with brain injury). Rapid
correction of low sodium (blood is hypotonic) can cause Central
Pontine Myelinolysis (potentially fatal). Rapid correction of hypernatremia
can cause cerebral edema. Rapid sodium changes cause rapid changes
Calculate Serum Osmolality =
2 (Na) + urea + glucose
Excessive mannitol use can produce dehydration. Dehydration can
increase CSF production and ICP. The goal is to maintain euvolemia.
The brain is totally dependent upon glucose as a source of energy.
Hypoglycemia causes energy depletion in the brain. Hyperglcyemia
is associated with poor neurological outcomes. Careful monitoring
Seizures increase brain metabolic rate and can lead to ischemic
injury if not treated promptly.
Monitor Intraventricular Pressure
The Clinical Nurse is responsible for the set-up, zeroing, leveling
and maintainance of an ICP monitoring circuit. Level transducer
to the external auditory meatus.
Prime set-up with normal saline, WITHOUT heparin and WITHOUT pressure.
See Procedure for Setting Up
Monitor waveform continuously. Record Mean ICP on neuro section
of flow sheet, q 1 h and prn. Position ICP drain at the level ordered
by the Neurosurgeon (e.g., 15 cm above the external auditory meatus).
Calculate CPP with each recorded ICP.
ICP drainage goal is ~ < 20 ml per hour. If drainage
exceeds this volume, or ICP is > ordered goal or drainage abruptly
stops, see Procedure for Troubleshooting
ICP and contact Neurosurgery if troubleshooting efforts fail
to resolve problems.
Clinical Nurses may gently aspirate ~ 1 ml CSF from the sampling
port closest to the patient for culture, with a physician's order. Procedure for CSF Sampling
Cerebral Pefusion Pressure (CPP)
= MBP - Mean ICP.
Normal ICP <10 mmHg.
Normal CPP = 60-80 mmHg. CPP < 50 mmHg may indicate
a signficant reduction in cerebral blood flow.
Monitor Lumbar CSF Pressure
The Clinical Nurse is responsible for the set-up, zeroing, leveling
and maintainance of a Lumbar CSF monitoring circuit. Level transducer
to iliac crest.
Prime set-up with normal saline, WITHOUT heparin and WITHOUT pressure. See Procedure for Setting Up
Lumbar Drainage System.
Assess dressing and drain at the start of each shift and document
in the 24 hour assessment record. Record Meand CSF pressure q 1
h on neuro section of CCTC flow sheet.
If pressure remains > 10-15 mmHg or goal ordered by physcian,
notify Vascular Surgeon.
Monitor pedal pulses, pain, sensation (pin and light touch) and
proprioception q 1 h X 24 hours. If normal function present, continue
to monitor q 2 - 4 h X 3 days or as ordered. Document findings in
spinal cord testing record.
Lumbar CSF is monitored following thoracic aneurysm
repair. Increased ICP > 10 mmHg suggests CSF flow obstruction
due to spinal cord ischemia. During thoracic aneurysm repair, cross
clamping requirements may compromise flow to the thoracic or lumbar
spine, leading to paraplegia.
Changes Introduced in 2014:
Target: Our standard temperature target has recently been revised to 34° - 36°C and this will be used in the majority of post cardiac arrest cases. On a case-by-case basis, we may decide to use the lower temperature target of 32 - 36°C, at the physician's discretion. The goal is to get the temperature in target as rapidly as possible after Return of Spontaneous Circulation (ROSC). The temperature should not exceed 36 °C.
While cooling was a key feature of clinical trials that examined hypothermia, all studies also utilized deep sedation and neuromuscular blockers if shivering occurred. We do not know whether it is the prevention of fever or deep sedation that provides the most protection, therefore, deep sedation with narcotic and a sedative (eg. propofol) is an essential part of the treatment. Fentanyl remains the agent of choice.
With the raising of the hypothermia target to 34° - 36°C, it is important to recognize that this does not mean than 36-36.5 is acceptable; the temperature must be below 36°C. Consider underlying sepsis among patients who do not cool quickly despite deep sedation and cold normal saline administration.
We have also switched to 500 ml bags of normal saline for cooling, but continue to give up to 4 Litres of fluid quickly for induction of hypothermia. The change to 500 ml ensures that the saline is still cold at the end of the infusion.
End of Cooling and Sedation:
The period of mild hypothermia is maintained for 24 hours (from the point when the temperature first dropped below 36°C. The new protocol extends the period of temperature control by providing antipyretics and/or cooling measures if required to keep the T < 37.5 for at last 72 hours.
The other change in the new protocol is the method for stopping the cooling protocol. Narcotics and sedatives are continued until 8 hours after the 24 hour cooling period has ended. At this point, narcotics and sedatives are stopped, but prn administration is continued to maintain patient comfort. Passive warming occurs as muscle activity resumes. Active rewarming is further delayed until 6 hours after the analgesic and sedative infusions are stopped..
- Initiate cooling as soon as bolus doses of
medications are administered.
Do not delay cooling for diagnostics, interventional cardiology, or to monitor for
- Rapidly (15 minutes) administer refrigerated 500 mL IV Sodium Chloride 0.9% boluses as soon as bolus medications are given. Repeat up to 4 L until target temperature achieved.
- Hold cooling if temperature less than target range.
- Wrap hands and feet with dry towels to prevent frost bite and to decrease shivering during period
of therapeutic hypothermia.
- If temperature above range, ice packs may be
added to the groin, axilla and /or neck area
- If patient is difficult to cool despite use of neuromuscular blocking agent, review with physician for possible underlying infection and need for cultures/antimicrobials
- Give cisatracurium bolus as per order for any of the following reason AFTER ensuring ANAESTHETIC doses of narcotic and sedatives (be careful not to administer NMBs is patient is under sedated):
- Muscle movement
- Ventilator triggering
- Temperature greater than target
- If recurrent/frequent doses are required to achieve goal, obtain an order to initiate an infusion of cisatracurium
- Be sure that analgesia and sedation are at anaesthetic dosing.
- Continuous core temperature by esophageal, bladder or pulmonary artery
- Ensure continuted FULL mechanical ventilation with complete support
- MD promptly if MAP < target if MAP < target to ensure adequate Cerebral Blood Flow
- Implement Standards of Care for a Patient receiving Neuromuscular Blockade
- Monitor ECG for arrhythmias during repositioning
or procedures, asymmtomatic bradycardia occurs as the temperature drops and often does not require treatment
- Ensure pacemaker pads are not in direct contact
with wet linen
- Assess skin for signs of frostbite q 2 hours and CONTINUE with Q2H turning and skin routine
- Continuous subhairline EEG to ensure patient is not having seizures
- Initiate enteral feeding, DVT prophylaxis, GI prophylaxis, VAP reduction protocols and intensive Insulin therapy. Avoid hyperthermia >37.5 for at least 72 hours
- Attempt to place feeding tube in small bowel; if small bowel placement unsuccessful, obtain order to initiate
gastric feeds at 10 mL/hour, as hypothermia increases risk for impaired gastric emptying.
- Administer Acetylsalicylic Acid (ASA), thrombolytics and anticoagulants as required to manage Acute Coronary
- If antiarrhythmic therapy is required, Amiodarone is recommended, unless contraindicated.
- Maintain target temperature for 24 hours once patient first achieved target
- 8 hours after the end of the cooling period, discontinue all sedative and analgesic infusions and
- Continue with PRN symptom management as required (if the patient has pain or becomes agitated; treat as per usual care)
- Passive rewarming is the goal; after sedation is stopped muscle activity should promote gradual correction
- Active rewarming with a cooling blanket can be considered 6 hours after the sedation has been stopped
- Maintain temperature < 37.5 for at least 72 hours; acetaminophen or cooling blankets may be required
In a recent (December 2013) clinical trial that included a larger sample size than the original two hypothermia trials, there was no difference in outcome between patients who received hypothermia at 34° - 36°C versus 32° - 34°C. Both groups received deep sedation.
Expeditious reduction in temperature correlates to neurological recovery. Avoid delay in cooling and achieve target quickly.
Initiate cooling immediately following Return of Spontaneous Circulation for any patient who is not completely alert. Do not delay cooling to assess for neurological improvement or for inteventions or tests.
The sooner the intervention is started, the greater the chance that brain cells will be preserved. Cooling can
be initiated up to 8 hours post event, but has its best impact when started STAT.
Administer ANAESTHETIC doses of narcotic and sedation as a rapid bolus. Once patient is deeply sedated (does not respond to a tap on the forehead), adminster the cisatracurium bolus. Cooling should commence as soon as the patient is given these boluses (don't wait for the infusion).
Begin cooling by the rapid and repeated administration of 500 mL boluses of Sodium Chloride, up to 4 Litres in total. The use of 500 mL bags ensures the bags are still cold at the end of the infusion. Ensure deep anaesthetic levels of narcotic and sedation and neuromuscular blockade until cooling is achieved.
Cerebral edema may be present following cardiac arrest. Hypotension reduces cerebral perfusion and should be avoided; discuss appropriate MAP goals for patient with physician to maintain
adequate cerebral perfusion pressure and provide “cerebral” resuscitation (consider whether patient has prior hypertension). In addition to facilitating cooling, the volume expansion helps to augment the MAP to ensure adequate cerebral perfusion. Vasopressors may be required.
Extremity wrapping decreases stimulation of thermoreceptors and prevents triggering of body rewarming responses.
Muscle activity increases heat production and metabolic rate. Administer neuromuscular blocking agents PRN for any
muscle activity during period of therapeutic hypothermia. If patient exhibits any signs of spontaneous movement or wakefullness, increase narcotic and sedation before NMB.
Underlying sepsis may make cooling more difficult. Cooling should be included in diffential diagnosis.
Rectal temperature monitoring can be used until PA or esophageal temperature monitoring is established. Rectal
temperature monitoring can be slow to reflect core changes, can be inaccurate when stool is in the rectum or if ice packs in
the groin come in contact with the probe.
Hypothermia studies used a regular dose of neuromuscular blockade. In the absence of any study that replicated these findings without NMB use, NMB are part of the protocol but may only be required PRN.
Full ventilation is required to reduce metabolic rate and support ventilation during high dose sedation and analgesia and intermittent or continuous neuromuscular bockade.