Tag: increased ICP causes

Primary brain injury can only be prevented through education and health promotion, and surviving the initial head injury is only a small part of the battle for the patient with a brain injury. Preventing secondary brain injury is even more important since it may have a greater influence on the final outcome than the primary brain injury itself. Throughout this blogpost we will go through ways of preventing secondary brain injury as much as possible.

Causes of Secondary Brain Injury

Causes of secondary brain injury include:

• hypoxia
• hypotension
• hypercapnia
• acidaemia
• anaemia
• intracranial mass
• hyperglycaemia OR hypoglycaemia
• hyperthermia OR hypothermia

• Preventing secondary brain injury is possible by preventing ALL mentioned causes through early treatment
• Most causes mentioned are related to raised ICP – Intracranial Pressure

The Monro-Kellie Hypothesis

The Monro-Kellie hypothesis states that the total volumes of brain (approximately 80%), CSF (approximately 10%) and intracerebral blood (approximately 10%) are constant. The cavity in which these three are housed a.k.a. the cranial cavity, is not able to expand, and so, an increase in one should cause a decrease in one or both of the remaining two. This ensures that the total volume of the three components remains fixed, and that no rise in ICP is caused.

ICP (Intracranial Pressure) is the pressure exerted by the intracranial contents against the skull. The brain normally is able to tolerate a significant increase in intracranial volume WITHOUT increasing much the ICP. If, however, this normal compensation mechanism becomes exhausted and the compliance limit is exceeded, an increase in ICP becomes imminent.

NOTE: an increase in ICP causes changes within the patient’s Vital Signs.

In normal circumstances, ICP is less than 10mmHg (in adults). If ICP increases to >20mmHg treatment is required!

Signs of Increased ICP

• unexplained changes in vital signs
• cushing’s triad – isolated systolic hypertension, bradycardia, and altered breathing patterns
• headache
• nausea & vomiting
• sensory deficits
• impaired motor function
• pupillary changes – if ICP >18mmHg
• altered level of consciousness
• decreased level of consciousness
• seizures

Cushing’s Triad

Monitoring Intracranial Pressure

Monitoring ICP can be done through the use of:

• ventriculostomy – intraventricular catheter
• subarachnoid bolt or screw
• subdural OR epidural catheter or sensor
• fibreoptic transducer-tipped intraparenchymal catheter
• non-invasive methods such as an automated IR pupillometry

Possible Causes of Increased ICP

Pathological Causes	Non-Pathological Causes
traumatic brain injury	coughing / sneezing
temperature	lifting / bending / body positioning
intra-thoracic pressure	stress / emotional responses
intra-abdominal pressure	pain
acidosis / hypoxia	blood pressure changes
lesions occupying space eg. bleeding, hydrocephalus, tumour, oedema, abscess, infection	valsalva manoeuvre

Factors affecting ICP

• MAP : Mean Arterial Pressure – both hypertension and hypotension may raise ICP
• Brain Trauma – expanding lesions increase ICP and may cause herniation a.k.a. brain matter displacement
• CMR Changes – Changes in Cerebral Metabolic Rate may happen due to hyperthermia and increase in blood flow to meet demands, which leads to an increase in ICP
• Conditions Causing Acidosis – results in cerebral vascular dilation such as hypoxia, ischaemia, and hypercapnia
• Increased Intra-Thoracic / Intra-Abdominal Pressure – may happen during coughing or suctioning and due to high PEEP
• Conditions Affecting Venous Return – pressure on jugular veins or patient positioning

Cerebral Perfusion Pressure

Cerebral Perfusion Pressure CPP is the difference between the MAP (Mean Arterial Pressure) and the ICP.

CPP = MAP – ICP

Ideally, CPP should be between 50-70mmHg, as this ensures an adequate blood supply to the brain. On the other hand, ICP should be approximately 10mmHg.

A decrease in CPP or rise in ICP may cause ischaemia, neuronal hypoxia, and even death.

NOTE: if MAP = ICP, cerebral blood flow may cease.

Preventing Rise in Intracranial Pressure

1. Control of Vital Signs

• HYPOTENSION reduces oxygen and nutrient perfusion; CPP = MAP – ICP; aim for MAP of >80mmHg to ensure CPP of >60mmHg with ICP of 20mmHg; to increase blood pressure administer fluids and vasopressors.
• HYPERTENSION may result following interventions or due to decreased cerebral perfusion; sedatives may help avoid blood pressure from increasing during procedures; primary anti-hypertensives such as beta blockers can be administered, but only if ICP is monitored, OR SBP is >180mmHg, OR MAP is >110mmHg; AVOID vasodilators as these increase ICP.

2. Ventilation

• HYPERCAPNIA causes vasodilation – a 30% increase in cerebral blood flow leads to a 10mmHg increase in PaCO2, which raises ICP.
• HYPOCAPNIA causes vasoconstriction, which in return reduces cerebral blood volume and ICP, leading to ischaemia.
• HYPOXIA causes cerebral vasodilation, leading to an increased intracranial blood volume and increased ICP (high levels of PaO2 have not shown evidence of any affect on CBF).
• GOOD OXYGENATION should be maintained (ideal SPO2 of >95% and PaO2 of >80mmHg), if needed, through intubation and mechanical ventilation. IMPORTANT – avoid high tidal volume (as this may cause acute lung injury) and use a low level of PEEP (5-8mmHg) to maintain good oxygenation.
• pH BALANCE should be maintained between 7.35 and 7.45
• AIM FOR LOW NORMAL PaCO2 (approx. 35mmHg) – although hyperventilation may be required temporarily to reduce cerebral vasodilation and enhance venous return; AVOID LOW PaCO2 as excessive vasoconstriction leads to ischaemia, restricting oxygen supply to the injured area, leading to an increase in damage.

3. Patient Positioning

• ELEVATE HEAD OF BED to about 30% – patient’s neck should be3 kept midline; gravity promotes CSF and venous drainage, resulting in a lowered ICP; NOTE: evidence as to whether or not bed elevation may lower CPP has been inconclusive in a recent systematic review (Alarcon et al., 2017).
• VENOUS RETURN OBSTRUCTION causes an increased ICP due to factors such as head rotation to one side, extreme flexion of arms and hips, neck angulation and pressure on jugular veins (eg. from tight ETT tie or lateral positioning), trendelburg positioning, and prone positioning.

4. Procedures & Environmental Factors

• SUCTIONING
• RAPID POSITION CHANGES
• PAIN & COUGHING
• VENEPUNCTURE
• REMOVING ADHESIVE TAPE
• USE OF BEDPANS/ENEMA

• AVOID ACTIVITY CLUSTERING and instead promote resting periods between procedures mentioned above. If needed, a short acting sedative may be administered as a bolus prior to the procedure.
• AVOID UNNECESSARY INSTRUMENTAL TOUCH & PAINFUL PROCEDURES
• REDUCE LIGHTING in the patient’s room
• REDUCE UNNECESSARY ENVIRONMENTAL NOISE such as unneeded alarms – set appropriately and in relation to the patient’s norms
• SUCTIONING increases intra-thoracic pressure, impedes venous return and increases ICP; hypoxia may lead to cerebral ischaemia. Reduce impact on the patient by providing hyperoxygenation before and/or after the procedure, hyperventilating, suctioning using a closed suction system, limiting the frequency and the duration of suctioning, administering a sedation bolus, or Lignocaine IV or via Tracheal Tube.

NOTE: Some studies have shown that the presence, touch, and voice of patient relatives may help decrease ICP. Other unrelated studies have also shown that oral hygiene, bed bathing, catheter care and chest percussion do not result in a significant rise in ICP.

Retrieved from http://www.learnpicu.com/neurology/ICP (left image) & http://pedsccm.org/FILE-CABINET/head_trauma/sld028.htm (right image) on 3rd January 2023

5. Sedation & Analgesia

• SEDATIVES, MUSCLE RELAXANTS & ANALGESICS can help reduce the effects of unpleasant procedures; Sedatives administered are usually opioids or benzodiazepines; Muscle relaxants should be avoided if possible, and should they be administered, ensure that the patient is sedated first.
• ADEQUATE VENTILATION may also be achieved through the effect of sedation and analgesia.
• ATTENTION!! Sedation and Analgesia may affect the MAP, leading to an affect on the CPP (cerebral perfusion pressure), thus, ensure adequate fluid volume. Similarly, sedation and analgesia may also mask certain aspects related to the neuro assessment, thus, for a patient on such medication, rely more on pupillary reaction rather than the neuro assessment.

6. Fluid Management

• In relation to OSMOTIC THERAPY, large molecules (eg. Mannitol) or Hyperosmolar solution (eg. hypertonic saline, which is considered to be superior and with less side effects) remain in circulation, increasing osmolarity. For osmosis to happen, an intact blood-brain-barrier is required, where fluid is drawn from diluted areas to more concentrated areas (from extracellular to intravascular space). This reduces cerebral oedema whilst improving blood flow.
• When administering osmotic therapy, CAREFUL MONITORING is required – monitor electrolyte levels especially Potassium and Sodium; replace fluid as necessary to avoid hypovolaemia; serum osmolarity should not exceed 320mOsm/L…higher levels may induce pulmonary oedema or rebound cerebral oedema.
• HYPERTHERMIA, unless infection is involved, may be induced by localised damage in the thermoregulatory centre within the hypothalamus. A 1°C rise in body temperature causes 6-10% increase in cerebral metabolic rate, increased oxygen demand, increased blood flow and volume due to vasodilation, and increased ICP. IMPORTANT: monitor the patient’s body temperature and help cooling by removing any extra blankets and administering antipyretics.
• THERAPEUTIC HYPOTHERMIA may reduce ICP, however, evidence of improved survival is still inconclusive to date. Additionally, avoid rapid cooling as shivering raises ICP, thus, should be prevented.

7. Seizure Control

• POST-TRAUMATIC SEIZURES happen in 5% of patients with head injuries.
• Seizures increase CEREBRAL METABOLIC DEMANDS: increased blood flow causes an increase in ICP; if flow doesn’t meet the cerebral metabolic demands, the patient experiences ischaemia and neuronal destruction.
• PHENYTOIN is considered to be an effective medication in the prevention of early seizures (always monitor serum levels when administering).

8. Nutrition & Elimination

• PROTEIN is very much required by a hypermetabolic brain.
• STRESS ULCER PROPHYLAXIS is commonly administered to patients with an increased risk of stress-related mucosal bleeding from the upper gastrointestinal tract. Apart from administering early enteral feeding, ideally through an orogastric tube, administer pharmacological prophylaxis such as H2-blockers, proton-pump inhibitors, or sucralfate.
• Attempt to maintain NORMOGLYCAEMIA – hyperglycaemia is associated with increased ICP, while hypoglycaemia is associated with aggravated brain injury. It’s also important to mention that intensive insulin therapy does not improve outcome, and may actually worsen the patient’s condition and prognosis.
• STOOL SOFTENERS may be required especially if the patient is constipated, since constipation increases intra-abdominal pressure and ICP.
• GASTRIC DECOMPRESSION is intended for patientS with gastric distention receiving aggressive ventilatory resuscitative measures prior to intubation. A NG tube may be used to perform gastric decompression for the patient with known or suspected gastric distension. Check tube placement. Attach suction or a large syringe and evacuate the stomach.NOTE: for patients with facial trauma use an orogastric tube instead.

In Summary…

List of Interventions to Minimise ICP

1. AIRWAY & VENTILATION

• monitor pH, pCO2 and pO2
• if GCS <9 ensure early intubation and mechanical ventilation
• avoid tight ETT or Tracheostomy ties
• avoid high PEEP
• suction only when necessary
• keep head elevated and aligned
• provide mouth care to eliminate oral secretions
• perform gastric decompression

2. ICP & CPP

• prevent rise in ICP
• prevent drop in CPP
• remember: CPP = MAP – ICP
• mannitol or furosemide may be administrated to reduce intracellular volume
• hypertonic saline reduces cerebral oedema whilst improving blood flow

3. NEUROLOGICAL & HAEMODYNAMIC MONITORING

• avoid drops in the patient’s blood pressure
• monitor the patient neurological status through the Glasgow Coma Scale and Pupil Reactivity

4. NUTRITION & FLUIDS

• ensure adequate nutrition and fluid intake as indicated
• fluid restriction may be indicated so as to prevent an increase in ICP
• monitor the patient’s electrolytes
• an adequate MAP can be achieved through administration of normal saline +/- inotropes
• monitor for diabetes insipidus (a rare condition which causes increased urination (polyuria) and increased thirst (polydipsia); Diabetes Insipidus is not related to type 1 or type 2 diabetes)

5. PREVENTION

• prevent hyperthermia
• prevent hyperglycaemia
• prevent hypoglycaemia
• prevent seizures
• prevent pain
• prevent anxiety
• prevent venous thromboembolism VTE

6. NEUROLOGICAL INTERVENTIONS

• an expanding haematoma may require ventriculostomy for CSF drainage and ICP monitoring
• craniectomy may also be indicated if an increase in space is required

7. PATIENT SAFETY

• ensure patient safety at all times

8. PSYCHOSOCIAL CARE

• promote congnitive function
• provide support to the patient’s relatives
• provide health literacy and rehabilitation advice to the patient and relatives

References

Alarcon, J. D., Rubiano, A. M., Okonkwo, D. O., Alarcón, J., Martinez-Zapata, M. J., Urrútia, G., & Bonfill Cosp, X. (2017). Elevation of the head during intensive care management in people with severe traumatic brain injury. The Cochrane database of systematic reviews, 12(12), CD009986. https://doi.org/10.1002/14651858.CD009986.pub2

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