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Brain Death Nawal Salahuddin MD, FCCP Associate Professor Section of Pulmonary & Critical Care Medicine AKUH

ICUs sometimes create an amalgam of Life-in-Death, A state of being unable to participate in human life but also unable to die

Historical perspective (1) The traditional concept of death emphasized cessation of respiration In 1978, Sweet stated in the New England Journal of Medicine; “ It is clear that a person is not dead unless his brain is dead. The time honored criteria of the stoppage of the heart beat and circulation are indicative of death only when they cause the brain to die”

Historical perspective (2) Death is a loss of Cellular Function that leads to putrefaction Death is an Irreversible cessation of the integrated functioning of the organization as a whole

Historical perspective (3) With organ transplantation, resuscitative techniques (artificial cardiopulmonary support, cryopreservation) the diagnosis of Brain Death has become especially important In 1981, the Uniform Determination of Death Act asserted the definition of Death as; “ 1. Irreversible cessation of circulatory and respiratory functions OR 2. Irreversible cessation of all functions of the entire brain, including the Brain Stem”

Pathophysiology: Relevent brainstem anatomy The primary Ventilatory Centre is located in the reticular core of the medulla oblongata. The circulatory system is controlled by central neurons diffused throughout the reticular core of the pons and medulla

Pathophysiology: Relevent brainstem anatomy The pupillary reflexes are mediated through the nuclei of cranial nerves II, III in the midbrain The Doll’s eye (oculocephalic) reflex & cold calorics (vestibulo-ocular) reflexes are mediated by cranial nerves VIII, II ,VI and the pontine reticular formation

Pathophysiology: Relevant brainstem anatomy Why are these reflex arcs important? These cranial nerve nuclei lie next to the RAS, which spans the midbrain & pons. The RAS is essential for consciousness and is not directly testable. If the adjacent nerve nuclei are not functioning there is no significant possibility that the RAS is intact

Causes of Brain Death 2 mechanisms; Global injury of the entire CNS Circulatory failure (cardiac arrest) Respiratory failure (anoxia from, CO poisoning) Focal injury to the CNS Primary Injury trauma, ischemia, IC heamorrhage Secondary injury (herniation of brain stem)

Definitions (1) Brain Death is defined as “ the complete & irreversible absence of all brain function”

Definitions (2) Important distinctions; Coma : Impaired consciousness either due to impairment of the RAS or cortex. Reversible Persistent Vegetative state : Cortices failed, brainstem functions Locked in Syndrome : Preserved upper brainstem functions (consciousness) preserved, lower brainstem impaired (respiration, circulation) Profound Hypothermia : can have clinical manifestations similar to brain death. So brain death cannot be diagnosed unless the core temperature is ≥ 32 º C

Brain Death implies failure of the Brain stem. There may also be associated failure of cortical functioning that leads to loss of integrative activity and brainstem reflexes

Prognosis Patients who fulfill criteria for brain death have; NO PROSPECT OF SURVIVAL independent of artificial respiratory & circulatory support, NO PROSPECT OF RECOVERY of brain function NO PROSPECT OF IMPROVEMENT even to a persistent vegetative state or coma

Diagnosis of brain death Clinical Criteria Confirmatory testing EEG Evoked responses Measurement of blood flow CT/ MRI Angiography Transcranial doppler ultrasound

Diagnosis of brain death: Clinical Criteria (1) Two preconditions must be met ; The cause of injury is known: there must be clear evidence of an acute, catastrophic, irreversible brain injury. Reversible conditions that may obfuscate the clinical diagnosis of brain death must be excluded. Body temperature must be greater than 32C, to rule out hypothermia. There is no chance of drug intoxication or neuromuscular blockade. The patient is not in shock.

Diagnosis of brain death: Clinical Criteria (2) The patient does not respond to verbal or visual command. The patient makes no movements, no spontaneous movements, or any movement induced by painful reflex. The pupils are fixed and nonreactive. The patient has no oculocephalic reflex. When the patient’s eyes are opened and the head is turned from side to side, the eyes remain fixed in their position. Alternatively, the oculovestibular reflex may be tested. The patient’s ear canal is inspected to ensure an intact tympanic membrane. While the eyes are held open, ice water is injected into the ear canal. The eyes of a brain-dead patient remain fixed in their position .

Diagnosis of brain death: Clinical Criteria (3) The patient has no corneal reflexes when a cotton swab is dragged across the cornea while the eye is held open. The patient has no gag reflex. The movement of the breathing tube (in and out) or insertion of a smaller tube down the breathing tube does not elicit a reflex. The patient has no spontaneous ventilation. The patient is temporarily removed from life support (the ventilator). With the cessation of breathing by the machine, the body immediately starts to build up metabolic waste of CO2 in the blood. When the CO2 level reaches 55 mm Hg, an active brain causes the patient to breathe spontaneously. A dead brain gives no response.

Diagnosis of brain death: Clinical Criteria (4) If, after this extensive clinical examination, the patient shows no sign of neurologic function and the cause of the injury is known, the patient can be pronounced brain-dead. more than one physician is required to make this pronouncement for brain death to become legal death. Although the patient has a dead brain and dead brainstem, spinal cord reflexes (eg, a knee jerk) can sometimes be elicited. In some brain-dead patients, a short reflex movement may occur when the hand or foot is touched

Diagnosis of brain death: Confirmatory testing (1) All these tests measure cortical activity in some way. Confirmatory tests are not generally required in the United States, but in several European, Central American, South American, and Asian countries, confirmatory testing is mandatory

Confirmatory testing(2): Electroencephalographic recording Loss of bioelectrical brain activity as shown on the EEG (ie, isoelectric EEG) is a reliable confirmation of whole-brain death. Total electrical silence is not required for brain death. It is important to note that an isoelectric EEG can be obtained after drug intoxication, such as intoxication with barbiturates and residual electrical activity may persist after BSD Electrocerebral inactivity or electrocerebral silence is defined as no EEG activity above 2 mV/mm.

Confirmatory testing (3): Evoked responses Brainstem auditory evoked potentials are signals generated at the level of the auditory nerves and brainstem in response to an acoustic stimulus. Brainstem auditory evoked potentials consist of five identifiable waves. Wave I represents the vestibular nerve action potential; wave II, the vestibular and cochlear nerves; wave III, the lower pons; and waves IV and V, the upper pons and the midbrain The loss of waves III to V or II to V, or no reproducible brainstem auditory evoked potentials on both sides, is usually regarded as indicating BSD Somatosensory evoked potentials are waves of neural activity generated from the neural structures along the afferent somatosensory pathways, which are generated after electrical stimulation of a peripheral nerve. The pathway starts at a peripheral nerve, then ascends by the brachial plexus, upper cervical cord, dorsal column nuclei, ventroposterior thalamus, and sensory cortex. Bilateral absence of specific waves following median nerve stimulation is consistent with brain death confirmatory laboratory finding

Confirmatory testing (4): Measurement of blood flow Absent intracranial circulation indicates irreversible cerebral damage Measurement of blood flow Angiography CT/ MRI Transcranial doppler ultrasound

Angiography. Absence of blood flow to the brain leads to destruction of brain tissue. The greatest advantage of angiography for the determination of brain death is that it is influenced neither by central nervous system– depressant drugs nor by hypothermia. CT. Various CT techniques may be used, including CT angiography, CT perfusion, and xenon-CT perfusion, to demonstrate absent or nonviable cortical blood flow MRI. MRI and magnetic resonance angiography should be used with caution in confirming brain death. Tran cranial Doppler sonography. Transcranial Doppler sonography uses a 2-MHz ultrasonic probe affixed to the temporal area, and the flow velocity of each of the major intracranial arteries may be measured. In brain death, cerebral perfusion pressure approaches zero, and transcranial Doppler demonstrates systolic spikes; undetectable flow (i.e., no signal); or reversal of blood flow in diastole (i.e., to-and-fro or oscillating waveform) .These patterns were highly specific for brain death

Sedation & Analgesia in the ICU Nawal Salahuddin MD, FCCP Associate Professor Section of Pulmonary & Critical Care Medicine AKUH

PAIN Control A sedated patient is not necessarily a pain-free patient Sources of pain; Surgical incisions, trauma Intravenous lines, bed sores, endotracheal suctioning Vertebral body fractures, arthritis, prolonged immobility Pain is misinterpreted as agitation

Adverse physiological effects of PAIN Increased endogenous catecholamines Myocardial ischemia Hyper metabolic states Sleep deprivation, agitation, anxiety, delirium

Analgesic Strategies Opiate receptors are found in the CNS & PNS. Clinically important receptors are designated µ & ĸ µ1 receptors mediate analgesia, µ2 receptors mediate respiratory depression, nausea, vomiting, constipation, euphoria

Analgesics(3) All opiates induce respiratory depression centrally mediated & dose dependent Response to hypercapnia is reduced Ventilatory response to hypoxia is obliterated These respiratory depressive effects are used in the ICU to treat ventilator-patient dyssynchrony, dyspnea , coughing

Analgesics(4) Opiates have minimal heamodynamic effects in euvolemic patients Hypotension is seen in patients whose BP is maintained by sympathetic compensation

Analgesics(5) Morphine-induced histamine release is rarely clinically important in the ICU Dependence & Withdrawal can be seen with prolonged infusions

Analgesics (6) Drugs most commonly used; Morphine Fentanyl Remifentanil Ketorolac

Recommendations for analgesic use in the ICU (1) All critically ill patients should have the right to adequate analgesia and management of their pain. Pain assessment and response to therapy should be performed regularly by using a scale appropriate to the patient population and systematically documented. Patients who cannot communicate should be assessed through subjective observation of pain-related behaviors (movement, facial expression, and posturing) and physiological indicators (heart rate, blood pressure, and respiratory rate) and the change in these parameters following analgesic therapy.

Recommendations for analgesic use in the ICU (2) A therapeutic plan and goal of analgesia should be established for each patient and communicated to all caregivers to ensure consistent analgesic therapy. If intravenous doses of an opioid analgesic are required, fentanyl, hydromorphone, and morphine are the recommended agents.

Recommendations for analgesic use in the ICU (3) Scheduled opioid doses or a continuous infusion is preferred over an “as needed” regimen to ensure consistent analgesia. Fentanyl is preferred for a rapid onset of analgesia in acutely distressed patients. Fentanyl or hydromorphone are preferred for patients with hemodynamic instability or renal insufficiency. Morphine and hydromorphone are preferred for intermittent therapy because of their longer duration of effect.

Recommendations for analgesic use in the ICU (4) NSAIDs or acetaminophen may be used as adjuncts to opioids in selected patients. Ketorolac therapy should be limited to a maximum of five days, with close monitoring for the development of renal insufficiency or gastrointestinal bleeding. Other NSAIDs may be used via the enteral route in appropriate patients.

Sedation: Indications Anxiety facilitate nursing care reduce Oxygen consumption & CO2 production When neuromuscular blockade is used

Sedation: Goals Should be individualized Sedation Scores Ramsay scale Sedation – Agitation scale Adaptation to ICU environment scale

Sedation: Drugs (1) Benzodiazepines act by potentiating the GABA receptor mediated inhibition of the CNS GABA receptors act by regulating a chloride channel on the cell membrane By increasing the intracellular flow of Cl - neurons become hyperpolarized with a higher threshold for excitability

Sedation: Drugs (2) All benzos are lipid soluble with a large volume of distribution Duration of action after a bolus is determined by the rate of redistribution to the adipose tissues

Sedation: Propofol(1) Propofol acts on the GABA receptor, although the site of action on the receptor is different from benzos Hydrophobic with high lipid solubility that allows for rapid crossing of the BBB and redistribution to peripheral tissues…. Rapid onset and short duration of action

Sedation: Propofol(2) It causes depressed responsiveness, anxiolysis and amnesia Ventilatory depression & apnea. NOT an analgesic Profound hypotension due to dilation of venous capacitance vessels & mild myocardial depression Hypertriglyceridemia; pancreatitis ‘ Propofol Infusion Syndrome’ : dysrhytmias, heart failure, metabolic acidosis, hyperkalemia & rhabdomyolysis. Associated with higher doses (> 80 mcg/kg/min.) or higher concentrations (2%) Not recommended in children

Sedation: Haloperidol Induce tranquility without respiratory depression Antagonize basal ganglia dopamine Doses of 1 – 10 mg. are used titrated to desired end – point. Onset 2 -5 min. , half life 2 hours Can prolong the QT interval on EKG, Neuroleptic Malignant Syndrome (lead-pipe rigidity, fever, mental status changes)

Recommendations for Sedative use in the ICU (1) Sedation of agitated critically ill patients should be started only after providing adequate analgesia and treating reversible physiological causes.

Recommendations for Sedative use in the ICU (2) A sedation goal or endpoint should be established and regularly redefined for each patient. The use of a validated sedation assessment scale is recommended. The titration of the sedative dose to a defined endpoint is recommended with systematic tapering of the dose or daily interruption with retitration to minimize prolonged sedative effects.

Recommendations for Sedative use in the ICU (3) Midazolam or diazepam should be used for rapid sedation of acutely agitated patients. Midazolam is recommended for short-term use only, as it produces unpredictable awakening and time to extubation when infusions continue longer than 48–72 hours.

Recommendations for Sedative use in the ICU (4) Propofol is the preferred sedative when rapid awakening (e.g., for neurologic assessment or extubation) is important. Triglyceride concentrations should be monitored after two days of propofol infusion, and total caloric intake from lipids should be included in the nutrition support prescription.

Recommendations for Sedative use in the ICU (5) The potential for opioid, benzodiazepine, and propofol withdrawal should be considered after high doses or more than approximately seven days of continuous therapy. Doses should be tapered systematically to prevent withdrawal symptoms.

Recommendations for Sedative use in the ICU (6) Haloperidol is the preferred agent for the treatment of delirium in critically ill patients. Patients should be monitored for electrocardiographic changes (QT interval prolongation and arrhythmias) when receiving haloperidol.

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