Although confusion is particularly common after significant head injuries, it is also not an uncommon occurrence after other types of trauma. It affects patients of any age, very young and elderly patients being particularly prone. The clinical finding of post-traumatic confusion should not be considered a diagnosis in itself, and requires appropriate clinical assessment and investigation to diagnose the causative pathology before the institution of a management regime appropriate to that particular pathology.
Aetiology and pathogenesis
Relatively minor head trauma is not infrequently overlooked in cases where there are significant other injuries. Although minor head injuries in themselves do not typically cause significant confusion, the effects of secondary brain injury in the post-traumatic period can rapidly develop into a relatively dangerous condition which often has confusion as its presenting symptom. Therefore, any post-traumatic confusion warrants specific clinical assessment and investigation to rule out potentially dangerous intracranial pathology.
However, it must be stressed that the exclusion of significant intracranial pathology is, in itself, insufficient investigation in a patient with post-traumatic confusion. Respiratory problems, metabolic derangements, infections and drugs can all be significant and potentially dangerous causes of post-traumatic confusion, and must be recognized and appropriately managed (Causes of post-traumatic confusion).
Management of patient with post-traumatic confusion
All patients with post-traumatic confusion require a full physical examination, including full neurological examination. Any suggestion of a reduction in conscious state of 2 or more GCS points (Table 66, “Glasgow coma score”), any focal neurological deficit, or any symptoms of meningism indicate a potential intracranial emergency. Particular attention must also be given to examination of respiratory system and for clinical evidence of sepsis.
|Score||opening (E)||Best verbal (V)||Best motor (M)||• Notes on GCS:|
|• GCS = E + V + M.|
|• Worst score is 3, best is 15.|
|• Use best response if differences between sides for eye opening or motor function.|
|• GCS measures only conscious state, not neurological deficit.|
|4||Spontaneous||Confused||Withdraws to pain|
|3||To speech||Inappropriate words||Abnormal flexion to pain (‘decorticate’)|
|2||To pain||Incomprehensible sounds||Extension to pain (‘decerebrate’)|
Investigation is dictated by the clinical history and examination findings. However, most cases of posttraumatic confusion require the following (Management of post-traumatic confusion):
- CT scan brain (urgent if GCS drop >2, or focal neurological signs)
- Arterial blood gas analysis (Pao2, Paco2, Bicarbonate, pH, base excess). Note that any patient with confusion must be suspected of having disturbances in respiratory function, and this must be excluded with arterial blood gas analysis. Skin oxygen saturation monitoring (pulse-oximetry) is a useful adjunct to monitor trends in patients with known ventilatory parameters, but is not an alternative to initial ABG analysis.
- Full blood examination (haemoglobin, RCC, WCC, platelets)
- Urea and electrolytes
- Consideration of septic work-up (if indicated clinically, and which may include wound swabs, blood cultures, urine analysis and culture, chest X-ray, lumbar puncture for CSF analysis).
General management of confused patient
Confused patients areConfused patients are generally best managed in a quiet environment, but need to be closely monitored by experienced nursing and medical staff. Agitated patients need to be protected from falls, etc., and bedsides are therefore essential. Padding to the bedsides, or even nursing on the floor on a thick mattress may provide more protection. On occasions physical restraints may be needed to protect the patient; however these must be checked regularly to ensure they do not cause pressure or pain or subject the patient to a risk for entanglement. It is essential that restraints are not used as a means to avoid close supervision; all confused patients need such supervision and those requiring restraint should be supervised even more diligently.
Familiar faces, such as family or close friends, may help relax a confused patient, although visitors and unfamiliar contacts should be kept to a minimum. Busy wards and noisy areas will often cause a confused patient to become quite agitated and are best avoided if possible.
Sedation is best avoided in confused patients if at all possible. The aim is to identify and treat the cause of the confusion rather than sedate the patient. Sedation may rarely be needed in an agitated patient where there is the risk of self-harm or injury. However, very often close supervision in a calm environment will allow sedation to be avoided. Sedation should only be used if significant intracranial and metabolic (particularly hypoxic) problems have been excluded. Sedation should never be used simply to facilitate easier nursing care. On the few occasions where sedation is needed it is most appropriate to use only short-acting parenteral (i.v.) sedatives in small doses titrated to effect. The clinician must constantly be aware of the potential for wrongly attributing decreased conscious state to sedative use, and missing a worsening and dangerous intracranial pathology or metabolic event.
Many patients with post-traumatic confusion have significant pain from other injuries. The pain often causes severe agitation, and the patient can be much better managed if appropriate analgesia is used. Narcotics have the side effects of altering conscious state, causing pupillary constriction and depressing ventilation, all of which are potentially catastrophic in a patient with a significant intracranial pathology. They have therefore historically been shunned by neurosurgeons. However, most modern neurosurgeons and traumatologists recognize the effective analgesic properties and the short and predictable action of narcotics when used by the i.v. route, and are prepared to use them cautiously. It must be stressed that only small, frequent i.v. doses (e.g. 1–2 mg morphine p.r.n.) should be used and these must be titrated carefully, with the patient closely supervised. Intramuscular doses have a more unpredictable and delayed action and should be avoided. The historical anachronism of using codeine instead of narcotics should be discarded; codeine is a narcotic with the same side effects as other narcotics when used in the same analgesic dose, but has the disadvantage of not being available in i.v. preparation. A note should be made that tramadol, which has recently been used increasingly in the management of severe pain, does increase the risk of seizures, and therefore is probably best avoided following head injury.
A confused patient is not competent to make appropriate important decisions. This of course includes giving consent for surgical procedures, and most countries have legal avenues which allow the clinician to undertake emergency medical procedures without consent. It must also be understood that a confused patient cannot competently discharge himself or herself from hospital against medical advice. The clinician must understand that the refusal of a confused patient to follow the clinician's advice is not done from a position of legal competency, and therefore the clinician maintains significant responsibility for consequences of these actions. On occasions, formal declaration of incompetency is required to allow appropriate care or restraint. However, in most cases even very confused patients can be quietly reasoned with and will follow gentle calm advice, particularly if people familiar to them are involved.
Specific management of the cause of confusion
The primary rule in management of a confused patient is to correct the primary cause of the confusion.
Any intracranial mass lesion (haematoma, hydrocephalus, brain swelling) identified on CT scan warrants an immediate neurosurgical opinion. Even patients managed in rural hospitals who are considered to have a relatively small lesion deserve the potential benefits of a telephone consultation between the managing clinician and a neurosurgeon. Whether the lesion requires surgical treatment (craniotomy in the case of an acute haematoma or burr-hole drainage of chronic subdural haematomas or hydrocephalus) depends primarily on the patient's clinical condition and the amount of mass effect of the lesion. Therefore, in a telephone consultation the most important information the neurosurgeon requires is the patient's GCS score, whether this has deteriorated and if so the rapidity of change, any focal neurological signs (e.g. pupillary inequality or unilateral change in motor function) and the amount of midline shift and asymmetry on the CT scan. Teleradiology can be a major benefit in these cases. Most neurosurgeons would generally advise surgical decompression of an accessible intracranial lesion, which causes more than a millimeter or two of midline shift, and would consider this to be relatively urgent if a patient is developing lateralising signs or has a deteriorating conscious state.
Hypoxia and respiratory disturbance
Oxygen supplementation must be used on confused patients until blood gas analysis results are available. Although relatively mild hypoxia or hypercarbia do not usually in themselves cause confusion, following a head injury they can seriously potentiate secondary brain injury and most neurosurgeons would advise maintenance of Pao2 of more than 100 mm Hg and Paco2 30–35 mm Hg. Hyperventilation is not usually recommended now following head injury as it has the potential to exacerbate cerebral ischaemia.
In a confused patient with a deteriorating conscious state it must be determined that not only is the airway patent and the patient has appropriate blood gases, but it needs to be ensured that the airway is protected by an intact and strong gag and cough reflex. If there is any doubt about the adequacy of airway patency or protection then endotracheal intubation becomes an immediate priority. If intubation is required in a trauma patient this must be done immediately, with the head and neck held in a neutral position by an assistant (spinal precautions), and should not be delayed for cervical radiology, brain scans or other investigations.
Electrolyte disturbances, particularly sodium anomalies, must be corrected with appropriate fluid and electrolyte therapy. A point of caution is that the rapid correction of long-standing hyponatraemia can cause central pontine myelinosis, and in this case the aim should be to correct slowly over 24–48 hours. More rapid correction of acute hyponatraemia (e.g. that caused by iatrogenic water intoxication) can be safely performed. Similarly, acute hyponatraemia caused by either SIADH or cerebral salt-wasting syndrome can be safely done relatively quickly. It needs to be recognised that while fluid restriction is appropriate for SIADH, salt-wasting syndromes are associated with total body water deficit. Expert endocrinology advice can be invaluable in these cases.
Infections, particularly pulmonary, urinary, wound or i.v.-line associated, are the most common causes of post-traumatic confusion after the first 24–48 hours. These must be considered in all cases, and a septic work-up performed. Meningitis must be suspected if confusion is associated with decreasing conscious state or meningism. In these cases lumbar puncture is mandatory. However, in a post-traumatic case an urgent cerebral CT is always advisable prior to lumbar puncture; intracranial mass lesions can mimic meningitis and can cause lumbar puncture to be a fatal procedure. If infection is clinically suspected, appropriate antibiotic therapy should be instituted after cultures are collected, and modified when culture and sensitivity results are known.