neurologic presentations in medical ICU

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Information about neurologic presentations in medical ICU

Published on May 12, 2010

Author: ranjithpolusani


Journal club : Journal club Dr Ranjith kumar Postgraduate in neurology Gandhi medical college Coma in non neurological intensive care units : Coma in non neurological intensive care units Santiago ortega et al University college of Wisconsin. The Neurologist,Nov,2009. Back ground : Back ground Increased survival among medical and surgical ICU. Increasing spectrum of illness secondary to critical illness 1/3 of icu patients,55% mortality rate Increase length of stay and disability Systematic approach to identify potentially reversible etiologies and prognostic factors Slide 4: Clinical history Physical examination Degree of sedation Neurologic examination Herniation syndromes Coma scales Essential clinical history in patients with loss of consciousness : Essential clinical history in patients with loss of consciousness History Time course-abrupt gradual fluctuating Preceding focal signs Previous episodes h/o recent illness h/o recent fall Altered behaviour Drugs Medical psychological history Alcohol drug abuse Possible causes SAH, seizure, bleeding Tumour, venous thrombosis Metabolic,subdural hematoma. Focal lesion TIA, seizure Infection, metabolic Subdural, epidural bleed Toxic, metabolic, infection Toxic-metabolic. Metabolic, psychiatric Toxic-metabolic Vital signs interpretation in comatose patients : Vital signs interpretation in comatose patients Vital signs Fever Hypothermia Hypertension Potential illnesses Infection, heatstroke, thyrotoxicosis, Drugingestion(cocaine,amphetamines,Tca,anticholinergic) Cold exposure, hypothyroidism, hypoglycemia, shock, Drugs(alcohol,barbiturates,opioids,sedatives) Pheochromocytoma, drugs (cocaine,amphetamine,phencyclidine) Vital signs interpretation in comatose patients : Vital signs interpretation in comatose patients Hypotension Tachycardia Bradycardia HTN-Bradycardia Addisons, sepsis, MI, Blood loss, hypothyroidism Alcohol, amphetamines, ethylene glycol Uremic coma, myxedema coma. Kocher-cushing reflex. Respiratory patterns in coma : Respiratory patterns in coma Cheyne stroke Kussmaul breathing Agonal gasps Central neurogenic hyprventilation Apneusis Cluster ataxic -Bihemispheric damage, metabolic -Metabolic acidosis, post mesencephalic lesions -Bilateral lower brainstem lesions -Bihemispheric,midbrain,pons -Lateral tegmentum of lower pons -Bihemispheric or pons -Dorsomedial medulla RAS Cutaneous and mucosal exam in comatose : Cutaneous and mucosal exam in comatose Petechiae &ecchymosis Hypermelanosis Cherry red skin Gray blue cyanosis Telangiectasia Ecthyma gangrenosum Splinter hemorrages pigmentedmacules TTP,ITP,DIC,RMSF,meningococcemia,vasculitis,endocarditis Addisons,chemotherapy,porphyria,melanoma .CO poisoning .Methemoglobinemia Chronic alcoholism,vascular malformations Pseudomonas sepsis Anemia,sepsis,leucemia,endocarditis Tuberous sclerosis,neurofibromatosis Neuro muscular blockers in ICU : Neuro muscular blockers in ICU Sedatives in ICU : Sedatives in ICU Evaluation of comatose : Evaluation of comatose Spontaneous activity, motor response, eye position and movements, pupillary reflexes, brainstem reflexes and asymmetry between right and left responses. Decorticate (flexor) posturing-lesion above level of red nucleus. Decerebrate posturing (extensor)-damage to lower midbrain or upperpons, severe damage and less chance of recovery. Ciliospinal reflex Main opthalmologic findings in comatose : Main opthalmologic findings in comatose Vitreous sub hyaloid haemorrages Papilledema,retinal exudates&haemorrages Papilledema Cholesterol embolus Subconjunctival hemorrage Periorbital eccymoses, Battle sign -SAH -hypertensive encepalopathy -ICT increase -carotid atheroma -endocarditis -head trauma Eye movements in coma : Eye movements in coma Conjugate horizontal roving Conjugate horizontal ocular deviation Wrong way eyes Downward ,inward eyes Ocular bobbing Ocular dipping Dysconjugate eye movemnts -Excludes midbrain, pons lesion -Contralateral pon/ipsilateral frontal -Paradoxically to,contralateral deep hemispheric leson. -Thalamic,upper midbrain lesion -Bilateral pontine damage -Diffuse cortical anoxia -Brainstem damage Abnormal pupillary responses in coma : Abnormal pupillary responses in coma Pupillary responses and coma : Pupillary responses and coma Glasgow coma scale : Glasgow coma scale FOUR score scale : FOUR score scale Eye response 4-eyelid open or opened, tracking or blinking to command 3-eyelids open, not tracking 2-eyelids closed, open to loud voice, not tracking 1-eyelids closed, open to pain, not tracking. 0-eyelids remain closed with pain Motor response 4-thumbs up, fist, or peace sign to command 3-localizing to pain 2-flexion response to pain 1-extensor posturing 0-no response to pain or generalized myoclonus/status Brainstem reflexes 4-pupil & corneal reflex present 3-open pupil wide & fixed 2-pupil/corneal reflexes absent 1-pupil & corneal reflex absent 0-absent pupil, corneal & cough reflexes Respiration 4-not intubated, regular breathing pattern 3-not intubated, cheyne-stokes breathing pattern 2-not intubated, irregular breathing pattern 1-breathes above ventilator rate 0-breathes at ventilator rate Cerebral herniation :clinical syndromes : Cerebral herniation :clinical syndromes Cerebral herniation clincal syndromes : Cerebral herniation clincal syndromes Differential diagnosis in non neurological ICU : Differential diagnosis in non neurological ICU Metabolic coma Structural coma major causes of organic coma-supra tentorial : major causes of organic coma-supra tentorial Unilateral Hemorrhagic contusion Subdural hematoma Epidural hematoma MCA occlusion & edema IC bleed Abscess tumor Bilateral Traumatic injury Multiple infarcts (vasculitis coagulopaty, cardiac emboli) Bilateral thalamic infarct Primary lymphoma ADEM Anoxia Metastases Leucoencephalopathy(chemotherapy,radiotherapy) Major causes of organic coma-infratentorial : Major causes of organic coma-infratentorial Brainstem pontine bleed basilar artery occlusion central pontine myelinolysis brainstem contusion Cerebellum cerebellar infarct cerebellar bleed cerebellar abscess cerebellar tumour Medical ICU : Medical ICU Metabolic encephalopathy-28.6% Seizures-28.1% Hypoxic ischemic encephalopathy-23.5% Stroke-22.1% Sepsis is major cause of neurological complication-38.8% Bleck et al-2 yr period Primary CNS processes : Primary CNS processes Acute stroke-1-4% in non neuro icu. Angiographic studies De clotting of Av shunts Vascular line insertions Air embolism Cardioversion Anticoagulation Thrombolytic therapy Primary CNS processes : Primary CNS processes Meningitis & encephalitis-change in mental state with fever, csf analysis and antibiotics. Posterior reversible leuco encephalopathy-acute hypertensive crisis involving brain, vaso genic edema, control with labetolol, nicardipine etc. Conditions associated with acute hypertensive crisis & hypertensive encephalopathy : Conditions associated with acute hypertensive crisis & hypertensive encephalopathy Toxemia of pregnancy Drugs-cyclosporine tacrolimus interferon fludarabine cisplatin gemcitabine erythropoetin Uncontrolled essential hypertension Secondary hypertension- SLE,AGN,CRF Primary CNS processes : Primary CNS processes New onset seizure-0.8-4%,focal most common. Myoclonic seizures-metabolic, drugs,hypoxia. Non convulsive status-10%(50%of TBI), 52% mortality in critically ill Myoclonic status epilepticus-12hrs of cardiac resuscitation, persists up to 48 hrs, poor prognostic sign, unresponsive to medication. Common precipitants of seizures in ICU : Common precipitants of seizures in ICU Metabolic: renal, hepatic, electrolyte, Endocrine Hypoxia/ischemia Sepsis Stroke Primary CNS inflammations Withdrawal delirium tremens BZD narcotics Drugs: Anti arrythmics- lidocaine, flecainide Antibiotics-imipenam, ciprofloxacin, norfloxacin, penicillin derivatives Antidepressants-amit, nortript,doxepin Bronchodilators-theophylline Immunosupressive drugs-cyclosporine,OTR3,FK506 Secondary CNS processes : Secondary CNS processes Encephalopathy is the most common neurological complication in medical ICU. Prolonged sedation Drug intoxication Sodium disturbances : Sodium disturbances Hypo natremia-incidence of1%,prevalence of 2.5%. Postoperative patients Lethargy, confusion, coma ,seizures. Central pontine myelinolysis Hypernatremia-increase use for ICT. Lethargy, obtundation, coma Progressive shrinkage of brain leading to cerebral vascular damage and sub dural hamatoma Calcium disturbance : Calcium disturbance Hyper calcemia- ionised calcium levels and rate of rise. Delirium, depression, coma. Hypo calcemia-commonly associated with sepsis. Irritabilty, tremors and seizures Magnesium disturbances : Magnesium disturbances Hypo magnesemia-commonly associated with hypo calcemia. Tremor, tetany, myoclonus and seizures. Hyper magnesemia- cns depression with lethargy, confusion and weakness. Serum levels>6meq/l causes coma Acid base disturbances : Acid base disturbances Severe acidemia-<7.2,metabolic,respiratory,mixed Increase of icp, decrease seizure thresold, stimulate chemoreceptor trigger zone. Severe acute alkalemia-ph>7.60 Cerebral vasoconstriction, decreased oxygen extraction Respiratory depression, tetany,coma,siezures renal : renal Uremic encephalopathy-BUN doubles, drowsiness, asterexis, myoclonus Post dialysis disequilibrium-rapid dialysis, first dialysis, extreme baseline pre dialysis BUN Younger patients, previous neurological deficits Cerebral edema along osmotic gradient Combative behavior, headache, myoclonic jerks, cramps, cortical blindness, coma, seizures Avoided by continuous veno venous hemodialysis liver : liver Acute hepatic failure-hyper ammonemia, hepatic encephalopathy. Gr IV -80% mortality pH dependent partial pressure of gaseous ammonia from blood Hypoglycemia/hyperglycemia-confusion, coma, seizures, focal neurological deficits. Hypoxic ischemic encephalopathy : Hypoxic ischemic encephalopathy Hypotension, hypoxemia, asphyxia, laryngeal edema Severity and duration of hypoxia Transient confusion, antegrade amnesia, focal, multi focal or global cns damage or brain death. Fixed pupils, myoclonic status, sustained upward gaze poor prognosis Delayed post anoxic encephalopathy Lucid interval of 1-4 weeks Diffuse hemispheric demyelination, cognitive cerebellar, pyramidal and coma. Sepsis encephalopathy : Sepsis encephalopathy Most common (70%) in medical icu. Highest mortality Multi organ failure Decreased cerebral O2 extraction ratios, disordered amino acid transport, micro abscesses, inflammatory mediators, dys regulation of neurotransmitters, direct cytotoxicity, disruption of blood brain barrier Surgical ICU : Surgical ICU Cholesterol embolisation-vascular catheterisation diffuse encephalopathy, retinal hemorrhage, transient hemiparesis, livedo reticularis, purple toes, renal failure, muscle weakness Muscle/renal biopsy-stacked needle shaped crystals Fat embolism-trauma and long bone fracture/surgery Multifocal ischemic stroke-Cardiothoracic surgery. watershed infarcts, LV thrombus, aortic atherosclerosis ,aortic cross clamping, infective endocarditis, arrythmias. MRI limited by pacemakers Transplant ICU : Transplant ICU Transplant organ/procedure related Immunosuppressive therapy Renal/liver transplantation : Renal/liver transplantation Cutaneous neuropathies ad spinal cord infarction Re vascularisation procedure BP changes Hyper coagulabilty-secondary to rapid correction of uremia Increase in ICT during postoperative anicteric phase Cardiac/BMT : Cardiac/BMT Single/multiple cerebral infarctions-emboli, global hypo perfusion, arrhythmias, bypass pump, supra therapeutic heparin Infections, Hippocampal damage Bmt-37% met encephalopathy, CNS infection with minimal signs cyclosporine : cyclosporine Tremor and restlessness Syndome1-confusion,cortical blindness, visual hallucinations Syndrome2-ataxia,cerebellar tremor, and focal weakness Within 2 weeks, IV,normal levels Psychosis, mutism, central pontine myelinolyis,actionmyoclonus. Tacrolimus/muromonab : Tacrolimus/muromonab Fine tremor, paresthesias, apraxia, aphasia, akinetic mutism. Cortical blindness, CIDP Aseptic meningitis and toxic encephalopathy Csf pleocytosis with neutrophil predominance, mild protein elevation, normal glucose and sterile cultures Seizures, psychosis, visual loss Offering prognosis : Offering prognosis Etiology, severity, secondary CNS damage, age. 5-pont Glasgow outcome scale,6-point pediatric cerebral performance category scale, GCS, FOUR score-motor score, sphincter conrol, self care, communication, pupillary reactivity Children and young adults, toxic or metabolic abnormalities-better Absence of brainstem reflexes, low GCS, hypoxia ,hypotension-worst MRI,MRS, DTI. Anoxic coma : Anoxic coma Pupils, corneal reflex, motor response to pain ,myoclonic status, SSEP, serum neuron specific enolase. No response or extension to pain, EEG with malignant characteristics, absent bilateral ssep-poor prognosis Elevated NSE at 24 and 48 hrs >33ng/ml -poor prognosis EEG with alternating high voltage slow waves with low voltage irregular fast activity-good prognosis Brain death and organ donation : Brain death and organ donation Irreversible loss of brain function including brainstem Traumatic brain injury and SAH Prerequisites to diagnosis Identify patients who are likely to progress to brain death Consent, ethical Optimize and treat any physiological disturbance associated with brain death to protect organs for transplantation hypothermia : hypothermia To minimize secondary brain damage Avoid hyperthermia-excito toxicity, free radical generation, inflammation, apoptosis. Therapeutic hypothermia-core body temp <33 c Massive ischemic stroke, TBI, anoxia External cooling devices, iv cold saline infusions, iv cooling catheters. Electrolyte abnormalities, cardiac arrhythmia,infection. Slide 49: Thank you

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