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Case 4 

Case 4
Chapter:
Case 4
Author(s):

Harutomo Hasegawa

, Matthew Crocker

, and Pawan Singh Minhas

DOI:
10.1093/med/9780199599837.003.0004
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A 58-year-old man was admitted after falling down a flight of concrete steps whilst drinking alcohol. On admission to the emergency department he smelt strongly of alcohol and complained of headache and neck pain. He was agitated and was attempting to climb off his trolley. He was disorientated but obeying commands (GCS E4, V4, M6), and his pupils were equal and reactive.

Questions

  1. 1. What are the priorities in the management of this patient?

  2. 2. How should his agitation be managed?

  3. 3. When is intubation indicated in a patient with a reduced level of consciousness?

  4. 4. The CT scan is shown in Fig. 4.1. Describe the findings on the scan.

  5. 5. How should this patient be managed?

  6. 6. One day after admission, he is no longer disorientated and feels well. He has no focal neurological deficits. He asks how long he needs to stay in hospital and whether any more tests are required. How would you answer his question?

  7. 7. The patient has a blood test prior to discharge (6 days into his admission) and his sodium level is 116mmol/L. He is alert and orientated.

    1. (a) What are the risks associated with hyponatraemia?

    2. (b) What is the likely diagnosis, and which investigations are required?

    3. (c) The results of the above investigations are as follows: plasma osmolality 265mmol/kg, urine osmolality 218mmol/kg, urine sodium 40mmol/L. He is clinically euvolaemic. How should he be managed?

Answers

1. What are the priorities in the management of this patient?

A rapid primary survey (airway with cervical spine immobilization, breathing, circulation) is required, followed by a CT scan of the brain to look for intracranial pathology. In trauma, the neck is frequently imaged at the same time to exclude cervical spine injuries. He will need a secondary survey in due course to ensure that no other injury has been missed.

2. How should his agitation be managed?

Patients with head injuries may be agitated for many reasons. The use of sedatives masks neurological deterioration and is not recommended in the acute setting. Specialist nurses are required to manage agitated patients with head injuries. Treating simple causes of agitation often proves effective (e.g. analgesia for pain, immobilizing/reducing a limb fracture, a urinary catheter for a full bladder). A small dose of promazine is often helpful in controlling agitation without adversely affecting the conscious state. Removal of the collar and blocks may help if the cervical spine is cleared.

3. When is intubation indicated in a patient with a reduced level of consciousness?

Intubation is indicated if the patient is unable to maintain their airway (and therefore is at risk of airway obstruction or aspiration) or if agitation renders essential supportive therapy (e.g. oxygen, intravenous fluids) or diagnostic investigations (CT scan) impossible. The decision must be made on an individual basis: a post-ictal patient with a GCS of 7/15 may not need intubation, whereas a patient with a GCS of 13/15 who is combative and needing a CT scan does.

4. The CT scan is shown in Fig. 4.1. Describe the findings on the scan (Fig. 4.2).

There are extensive bifrontal contusions (A). The hypodense areas surrounding the blood (B) are indicative of oedema. Traumatic subarachnoid haemorrhage is also present (C).

5. How should this patient be managed?

This patient requires admission to the neurosurgical unit for close observation. Sodium levels, clotting, and liver function should be checked, the latter in view of the history of alcohol use. Anticonvulsants are recommended for one week after severe traumatic brain injuries and then discontinued if there has not been a seizure (see ‘Anticonvulsants in neurosurgery’, [link]).

6. One day after admission, he is no longer disorientated and feels well. He has no focal neurological deficits. He asks how long he needs to stay in hospital and whether any more tests are required. How would you answer his question?

The scan shows sizeable contusions with surrounding oedema. Cerebral oedema around evolving contusions is maximal 24–48 hours after the injury, but can also manifest several days after the injury and lead to neurological decline. A further period of hospital observation would be recommended for this patient (typically a few days). He should have a repeat CT scan and his serum electrolytes should be tested prior to discharge.

7. The patient has a blood test prior to discharge (6 days into his admission) and his sodium level is 116mmol/L. He is alert and orientated.

(a) What are the risks associated with hyponatraemia?

Altered mental state, seizures, cerebral oedema, and death.

(b) What is the likely diagnosis, and which investigations are required?

Hyponatraemia in neurosurgery is commonly due to the syndrome of inappropriate ADH secretion (SIADH) or cerebral salt wasting (CSW). Plasma osmolality, urine osmolality, and urine sodium concentration should be checked to exclude other causes of hyponatraemia. A clinical assessment of the extracellular volume status of the patient should be made to determine if the diagnosis is more likely to be SIADH (euvolaemic or hypervolaemic) or CSW (hypovolaemic).

(c) The results of the above investigations are as follows: plasma osmolality 265mmol/kg, urine osmolality 218mmol/kg, urine sodium 40mmol/L. He is clinically euvolaemic. How should he be managed?

The management of a hyponatraemic patient with a clinical picture consistent with both SIADH and CSW is controversial. This patient was managed with fluid restriction in the high-dependency unit and his sodium level normalized over a period of 72 hours (see ‘Hyponatraemia in neurosurgery’, [link]).

Further reading

Rahman M, Friedman WA (2009). Hyponatremia in neurosurgical patients: clinical guidelines development. Neurosurgery; 65: 925–36.Find this resource:

Hyponatraemia in neurosurgery

Initial tests in a hyponatraemic neurosurgical patient should include plasma osmolality, urine osmolality, and urine sodium concentration to determine the cause of hyponatraemia (Fig. 4.3). SIADH and CSW are common in neurosurgery. Both are characterized by low plasma osmolality, high urine osmolality, and high urine sodium concentration. Assessment of the extracellular volume (ECV) status may be helpful in distinguishing between them, although this is not always reliable. A patient with CSW is expected to be dehydrated whereas a patient with SIADH will be expected to be euvolaemic or hypervolaemic, but most patients do not lie on the clinical extremes. SIADH is relatively more common in head injuries and CSW in subarachnoid haemorrhage, although both can occur in either diagnosis. Another common cause of hyponatraemia is cortisol deficiency following pituitary surgery.

Fig. 4.3 Diagnostic approach to hyponatraemia in neurosurgery.

Fig. 4.3
Diagnostic approach to hyponatraemia in neurosurgery.

Management is guided by the magnitude of hyponatraemia, the underlying diagnosis, and clinical symptoms of hyponatraemia. If the patient is symptomatic, immediate salt and water replacement with intravenous hypertonic saline is required. If the patient is asymptomatic and/or the hyponatraemia is relatively mild, either salt and water replacement or fluid restriction can be trialled, although fluid restriction is not advised in subarachnoid haemorrhage as it may precipitate cerebral ischaemia. Whichever approach is adopted, the sodium concentration should not be raised abruptly (typically not more than 8mmol/L in 24 hours) in order to avoid central pontine myelinolysis. An endocrinology opinion should be considered.

Syndrome of inappropriate ADH secretion (SIADH)

The hypothalamic osmoreceptors detect changes in plasma osmolality and in response secrete antidiuretic hormone (ADH). ADH alters the water permeability of the collecting ducts in the kidney. More ADH results in more aquaporins in the kidney collecting ducts, leading to increased water reabsorption independent of sodium reabsorption. In SIADH there is excess water reabsorption, leading to a low-volume concentrated urine and relatively increased plasma volume. The plasma sodium and osmolality are low (due to dilution), and urine osmolality is high. Total urinary sodium excretion is normal but the urine sodium concentration is increased due to the low urine volume. Treatment is to limit or decrease the plasma volume with fluid restriction or diuretics. If the patient is symptomatic, the priority is to increase the plasma sodium level, and intravenous salt supplementation is indicated (this outweighs the increase in plasma volume due to the sodium infusion).

Cerebral salt wasting (CSW)

Although the pathophysiology of this condition is not completely understood, it is thought to result from impaired sodium reabsorption in the kidney leading to net sodium loss and therefore water loss. This leads to hyponatraemia with low plasma osmolality and high (or normal) urine osmolality. It is of particular concern following subarachnoid haemorrhage, and in conjunction with cerebral arterial vasospasm is a major cause of delayed neurological deterioration after the haemorrhage. The patient is clinically dehydrated and treatment is with aggressive salt and fluid supplementation. Fludrocortisone increases sodium and water retention in the kidney and is often used to manage this condition.

Anticonvulsants in neurosurgery

Common clinical questions are:
  • Are anticonvulsants indicated?

  • Which one should be used?

  • How long should it be continued?

  • Do levels need to be monitored and if so when?

  • What action is required if levels are sub-therapeutic?

Most of the literature concerns particular groups of patients and/or drugs or includes a diverse group of patients and/or drugs, so applying the conclusions to individual patients is difficult. This is clearly reflected in the case of brain tumours (see below). Some published guidance is summarized in Table 4.1. Patients with a central nervous system lesion who have a seizure satisfy the diagnosis of epilepsy and should be managed as such.

Table 4.1 Anticonvulsant use in neurosurgery

Condition

Seizure risk

Setting

Guidance

Brain tumour

Depends on tumour type and location: up to 100% for DNETs, 75% for low-grade astrocytomas, 50–60% for high-grade astrocytomas.1

Prophylaxis

See below

Treatment after seizure

Treat as epilepsy. Non-enzyme inducers (e.g. levetiracetam) do not affect the efficacy of corticosteroids and chemotherapy and may be preferred.1 Continue for as long as tumour is present; may taper after resection.

Traumatic brain injury

Depends on severity.

15% with severe TBI.

Risk increased (〉20%) in penetrating injury, depressed skull fracture, early seizure, subdural haematoma.2

Prophylaxis

Phenytoin for 1 week prevents early (〈7 days) seizures although this has no effect on outcome.3

Treatment after seizure

Treat as epilepsy. No specific guidance exists for traumatic brain injury.2

Subarachnoid haemorrhage

5–8%4

Prophylaxis

Generally not recommended5,6 as prophylactic phenytoin use has been associated with worse outcomes although newer drugs have not been fully assessed.

Treatment after seizure

Treat as per epilepsy, with drug other than phenytoin.6

Spontaneous intracerebral haemorrhage

2.7–17%7

Prophylaxis

Not recommended, as prophylactic anticonvulsants (mostly phenytoin) have been associated with worse outcomes.7

Treatment after seizure

Treat as epilepsy.7

Fitting neurosurgical patient: acute treatment

The seizure should be terminated with a benzodiazepine following which an anticonvulsant should be instituted. The drug of choice is one which attains a therapeutic effect rapidly and can be given intravenously if swallowing is not possible. The traditional choice is phenytoin, but levetiracetam and sodium valproate (neither of which require serum-level monitoring) are alternatives. If phenytoin is used in the acute situation an initial level can be taken after 1 hour to determine the subsequent dose or need for reloading. An alternative drug should be instituted if long-term therapy is indicated in order to avoid the side effects of phenytoin.

DNET, dysembryoplastic neuroepithelial tumour.

3 Brain Trauma Association 2007

Seizure prophylaxis in brain tumours

Meta-analyses (Glantz et al. 2000; Sirven et al. 2004; Tremont-Lukats et al. 2008) based on four randomized studies (see Table 4.2) and a cohort study (Forsyth 2003) do not recommend seizure prophylaxis in patients with brain tumours because of lack of efficacy and morbidity from medication side effects, but this conclusion has limitations. First, the randomized studies include a wide variety of tumours and non-neoplastic pathologies and do not apply to an individual patient whose seizure risk should be assessed individually based on the type and location of the tumour. Secondly, the anticonvulsants studied were limited to phenytoin, phenobarbital, and sodium valproate. Thirdly, many patients (up to 67%) had sub-therapeutic drug levels at the time of seizure. Therefore decisions about prophylactic anticonvulsant treatment in patients with brain tumours must be tailored to the individual and not based solely on recommendations from meta-analyses.

Table 4.2 Randomized studies of seizure prophylaxis in brain tumours

Study

Diagnosis (no. of subjects)

Anticonvulsant used

Percentage sub-therapeutic at time of seizure

Percentage side effects in drug group

Median follow-up

Glantz et al. (1996)

(RCT, n = 74)

Metastasis (57)

NHL (2)

GBM (9)

Other (6)

Sodium valproate

23%

5%

7 months

Franceschetti et al. (1990)

(RCT, n = 63)

Meningioma (27)

GBM (23)

Metastasis (13)

Phenytoin Phenobarbitone

67%

10%

6–12 months

Lee et al. (1989)

(RCT, n = 80 for tumours, n =374 for whole study)

Meningioma (50)

Glioma (30)

Aneurysm (41)

ICH (18)

AVM (12)

Metastasis (5)

Head trauma (210)

Others (8)

Phenytoin

50%

Not indicated

1.5 days

North et al. (1983)

(RCT, n=81 for tumours, n=281 for whole study)

Meningioma (19)

Metastasis (13)

Glioma (32)

Sellar tumour (17)

Aneurysm (55)

Head trauma (100)

VP shunt (25)

Other (20)

Phenytoin

Not indicated

Not indicated

Not indicated

Forsyth et al. (2003)

(cohort study, n = 100, including 28 infratentorial)

GBM (28)

Low-grade glioma (3)

Anaplastic glioma (9)

Metastasis (60)

Phenytoin

Phenobarbital

47% non-compliant at predetermined test time (not at time of seizure)

13%

5.4 months

RCT, randomized controlled trial; NHL, non-Hodgkin lymphoma; GBM, glioblastoma multiforme; ICH, intracranial haemorrhage; AVM, arteriovenous malformation; VP, ventriculoperitoneal.

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