Send the link below via email or IMCopy
Present to your audienceStart remote presentation
- Invited audience members will follow you as you navigate and present
- People invited to a presentation do not need a Prezi account
- This link expires 10 minutes after you close the presentation
- A maximum of 30 users can follow your presentation
- Learn more about this feature in our knowledge base article
Do you really want to delete this prezi?
Neither you, nor the coeditors you shared it with will be able to recover it again.
Make your likes visible on Facebook?
You can change this under Settings & Account at any time.
Brainstem death & coma
Transcript of Brainstem death & coma
Hypoxic-Ischemic brain injur
Coma Persistant vegetative state Minimally conscious state Brain stem death
GLASCOW COMA SCALE
Persistent vegetative state: unawareness, but in which patients have normal sleep-wake cycles and are arousable.
Brain Death: irreversible cessation of cerebral and brainstem function.
no respiratory drive, and thus there are no spontaneous breaths regardless of hypercarbia or hypoxemia.
no responses arising from the brain (including cranial nerve reflexes and motor responses) to stimuli, although spinal reflexes may persist
coma: pathological unresponsivness, caused by either dysfunction of the reticular activating system above the level of the mid-pons, or dysfunction of both cerebral hemispheres.
Minimaly consciousness state: severe alteration in consciousness, with intermittent and limited imited interaction with the environment by visually tracking, following simple commands, signaling yes or no (not necessarily accurately), or having intelligible verbalization or restricted purposeful behavior.
Persistent vegetative state
What was the time course of the loss of consciousness? abrupt (eg, subarachnoid hemorrhage, seizure), gradual (eg, brain tumor), or fluctuating (eg, recurring seizures, subdural hematoma, metabolic encephalopathy)?
Did focal signs or symptoms precede the loss of consciousness? As an hemiparesis suggests a structural lesion, likely with mass effect. Transient visual symptoms, eg, diplopia or vertigo, suggest ischemia in the posterior circulation.
Did the patient have previous neurologic episodes that suggest transient ischemic attacks or seizures?
What recent illness has the patient had? Has there been altered behavior or function recently? A fever suggests infection; an increasing headache suggests an expanding intracranial lesion, infection, or venous sinus thrombosis; recent falls raise the possibility of a subdural hematoma; recent confusion or delirium might indicate a metabolic or toxic cause.
What prescription or nonprescription drugs are used? Are there medical or psychiatric conditions? Is there history of alcohol or drug abuse?
●Ventilatory pattern —
leukoencephalopathy syndrome, hypertensive encephalopathy, or hypertensive intracerebral/cerebellar/brainstem hemorrhage.
BP: sepsis, hypovolemia, or cardiac failure, as well as certain drugs or Addison's disease.
Cerebrospinal fluid rhinorrhea can occur with skull fracture,
Petechiae and ecchymoses can be seen in bleeding diatheses (eg, thrombocytopenia, disseminated intravascular coagulation), some infections (eg, meningococcal septicemia, Rocky Mountain spotted fever), and certain vasculitides. Subungual (splinter) and conjunctival hemorrhages are sometimes seen in endocarditis. Petechiae confined to the head and neck may be found after convulsive seizures due to acutely raised venous pressure.
Resistance to passive neck flexion suggests meningismus, a sign of meningeal irritation occurs in meningitis and subarachnoid hemorrhage.
Level of consciousness
●Brainstem reflexes: pupillary light, extraocular, and corneal reflexes
Corneal reflex — The corneal reflex's afferent limb arises from small unmyelinated pain fibers in the cornea, the fifth or trigeminal nerve and nucleus, and activates the dorsal parts of both facial nuclei in the pons. Hence, both orbicularis oculi muscles contract when either cornea is touched. There are also connections with the oculomotor nucleus, so that the eyeballs move upward in concert with lid closure.
There are a number of prerequisites before one can begin considering a patient "brain dead" :
Clinical or neuroimaging evidence of an acute CNS catastrophe.
●Exclusion of complicating medical conditions that may confound clinical assessment (no severe electrolyte, acid-base, endocrine, or circulatory (ie, shock) disturbance).
●No drug intoxication or poisoning, which may confound the clinical assessment.
●Core temperature >36ºC (97ºF).
Normal systolic blood pressure >100 mm Hg.