COMELE

DEFINITIE: pierderea starii de constienta; stare asemanatoare somnului din care bolnavul nu poate fi trezit, ochii sunt inchisi si raman inchisi in ciuda aplicarii de stimuli puternici Constienta: forma cea mai inalta de reflectare a realitatii proprie omului, produs al creierului uman in procesul muncii, al vietii in societate, caracterizata prin prezenta gandirii si a limbajului, prin faptul ca omul isi da seama de lumea inconjuratoare si actioneaza asupra acesteia in conformitate cu anumite scopuri dinainte stabilite (Dictionarul limbii romane). Prezenta constientei depinde de integritatea anatomica si functionala a : -sistemului reticulat activator (SRA): -incepe in portiunea medie a puntii lui Varolio -urca in partea dorsala a mezencefalului -sinapsa in thalamus, de unde pleaca fibrele talamo- corticale -proiectiilor corticale (C) FIZIOPATOLOGIE. Integritatea anatomica si functionala a SRA si C poate fi pierduta prin boli: - ale sistemului nervos:iritatie meningeala leziuni de masa ale emisferelor cerebrale leziuni de masa ale mezenceflului convulsii generalizate - metabolice: intoxicatii (CO, benzodiazepine, opioide, etc) Insuficienta hepatica Coma acido-cetozica din diabet Coma hipoglicemica Coma din tulburarile hidro-electrolitice si acido-bazice Hiponatremie cu hipervolemie si hiperhidratare cerebrala Acidoza metbolica (insuficienta renala) Acidoza respiratorie (insuficienta respiratorie) Iritatia meningeala: inflamatie, infectie, hemoragie subarahnoidiana (ultimile 2 pot sa nu prezinte elemente dg la CT) Mecanisme discutabile: • eliberarea de citochine si interleukine care cresc permeabilitatea membranei hematoencefalice (IL-1, TNF, metabolite ai acidului arahidonic) • sinteza crescuta de radicali liberi de O si de NO • edem cerebral vasogen • alterarea fluxului sanguine cerebral • cresterea sintezei de aminoacizi neurotransmitatori excitatori neurotoxici • tardiv: vasculita si tromboza a venelor meningeale, urmata de necroza difuza corticala si a substantei albe Leziuni de masa emisferice: Se extind spre:

fasciculul longitudinal medial traverseaza SR ) Apar semne clinice de lateralitate Un bolnav comatos fara afectarea miscarilor reflexe de lateralitate ale globilor oculari nu are leziuni de masa mezencefalice in fosa posterioara CT poate san u detecteze unele leziuni din fosa posterioara. Apar semne neurologice de lateralitate Leziunile au elemente diagnostice la CT. Leziuni de masa mezencefalice: Comprima direct SRA Leziunile de fosa posterioara pot compromite functia cerebrala prin herniere in sus prin cortul cerebelului. blocand fluxul LCR din ventriculii laterali: hidrocefalie necomunicanta (cefalee intensa) Sunt afectate miscarile reflexe ale globilor oculari: centri pontini oculomoteri.• linia mediana si emisferul opus pe care il comprima sau comprima SRA rostrala: hernie laterala • mezencefal. dar mai ales cand ele coexista. Convulsii generalizate: descarcare electrica anormala. difuza in SRA si cortex In faza postcritica apare o inhibitie a activitatii electrice-coma Coma postcritica apare mai ales la cei care fac convulsii pe un fond patologic al SNC Anomalii metabolice: toxicele exogene sau endogene afecteaza SRA Nu exista semne neurologice de lateralitate Coma cu paralizia miscarilor reflexe oculare Nu exista elemente diagnostice la CT COME CU CT CRANIAN NORMAL Cauze meningee: hemoragie subarahnoidiana (rar) Meningita bacteriana Encefalita Empiem subdural Toxine exogene: sedative sau barbiturice Anestezice sau gamahidroxibutirat . nucleul n. care separa compartimentul emisferelor cerebrale de mezencefal si fosa posterioara: hernie transtentoriala Coma apare in fiecare din aceste situatii. lll. prin cortul cerebelului.

“spike-wave stupor” Hipothermia sau hiperthermia Boli multifocale manifestate cu coma metabolica: CID. vasculita. narcoza) Convulsii : status postictal prelungit. salivatie. AVC (coma apopolectica. bronhoree. supradoza apare cand se administreaza pentru a trata sevrajul la opiacee Clinica: ANAMNEZA. encefalopatie uremica. de 2-3 ore. embolii grasoase. hiponatremie. fibrilatie atriala: embolie cerebrala • Diabet zaharat: coma hipoglicemica. prin leziuni de macro si microangiopatie cerebrale) • Ciroza hepatica: coma hepatica (insuficienta hepatica). cian. coma hiperosmolara (hiperglicemie fara acido-cetoza). cu mentinerea semnelor vitale • Coma asociata cu agenti colinergici: lacrimare. pancreatita. hipertermie • Clonidina este activa pe sistemul de receptori opioizi. sepsis. AVC hemoragic • Insuficienta renala: coma uremica • Valvulopatii.Alcool Stimulante: phencyclidine. deficiente sau deranjamente: Hipoxie sau ischemie Hipoglicemie Hipercalcemie Osmolar: hiperglicemie. AVC ischemic. lithium Anticonvulsivante Opioide Clonidina Peniciline Salicilati Anticholinergice Monoxid de carbon. methemoglobina Toxice endogene. purpura trombotica trombocitopenica. coma hipoglicemica. coma profunda (scala Glasgow 3). coma acido-cetozica. insuficienta pulmonara ( hipercapnie. coma hiponatremica . adesea cu miscari mioclonice sau confuzie. phenophiazine. hipernatremie Insuficienta organica: encefalopatie hepatica. medicamentele de revigorare si de body-building duc la coma caracterizata prin debut si iesire din coma rapide. encefalopatia hipertensiva. micrometastaze difuze Ischemia mezencefalica AVC de trunchi basilar Hemoragie mezencefalica sau cerebeloasa NB: • Anestezicele generale similare cu acidul gama-aminobutiric pot induce coma. Antecedente patologice: • HTA: encefalopatie hipertensiva. cocaine sau amphetamine Medicamente psihotrope: antidepresive ciclice.

Rapid. intoxicatia barbiturica. purpura trombotica trombocitopenica (PTT) • Vasculite cu determinari vasculare cerebrale Simptome care preced instalarea comei: • Cefalee: acuta. tumori cerebrale lent evolutive. meningita. EXAMEN CLINIC GENERAL: • Tegumente: umede: hipoglicemie.medicamente. encefalita. tromboflebita Debut. endocardita bacteriana. procese expansive. procese chistice de ventricul lll coma hipoglicemica • Lent. meningte. mixedem • Culoarea tegumentelor: cianoza: coma hipercapnica. coma hipoglicemica. malformatii vasculare ce au produs si crizele epileptice • Intoxicatii :CO. brusc minute-ore : coma vasculara-hemoragie subarahnoidiana sau intraparenchimatoasa. hipotermie drept cauza comei COMELE PROFUNDE: HIPERTERMIE IN PLATOU. encefalita Metabolice: cu exceptia comei hipoglicemice. cianoza roz: CO icter: insuficienta hepatica teroasa: uremia hiperpigmentata predominant la pliuri: insuficienta suprarenala • Hemoragii cutanate: o Petesii. meningite • Sepsis. insuficienta renala • Temperatura: febra: infectii. (de ex: intoxicatie cu CO) • Neoplazii: metastaze cerebrale • Epilepsie: coma postcriza. hemoragie intraparenchimatoasa. infectii (+ febra). hemoragie subarahnoidiana.Insuficienta respiratorie cronica: coma hipercapnica Insuficienta respiratorie acuta: coma prin hipoxie si/sau hipercapnie acute. ore-zile: Neurologice: AVC ischemice. intoxicatia alcoolica. droguri • Fracturi: embolii grasoase • Infectii locale: encefalite. dramatica: hemoragie subarahnoidiana sau intraparenchimatoasa cronica: tumora cerebrala • Agitatie: intoxicatie alcoolica. hipocapnie (inversarea ritmului somn /veghe. ocluzia trunchiului bazilar scazuta: coma diabetica. purpura + febra: meningoencefalita meningococica o Echimoze: coma traumatica • Edem gambier sau extins: insuficienta cardiaca. hemoragie intratumorala. coma renala. CU CARACTER PROGRESIV • • • . encefalite. pancreatita. deshidratare. purpura: coma hepatica. sevraj medicamentos • Tulburari de comportament: encefalopatie hepatica. coma hipotiroidiana. PTT o Petesii. CID. intoxicatie cu anticolinergice Uscate: coma diabetica. hipoxie. flapping tremor) • Convulsii focale: leziuni supratentoriale: tumori. intoxicatia CO.

leziune pontina cu localizare joasa o Respiratie ataxica: ritm complet neregulat. soc hemoragic. insuficienta suprarenala COMELE PROFUNDE: HTA + PULS BRADICARDIC. hemoragii subarahnoidiene sau in parenchim. rino sau otolicvoree • Respiratia: o Apnee posthiperventilatorie: apnee de 15-30 sec dupa 5-6 respiratii fortate. echimoza retroauriculara (semnul Battle-asociat cu fractura bazei craniului). Bradicardie: hemoragie intracerebrala. amplitudine variabila de la o miscare la alta. regulate. se ineaca): lez la nuclei X-Xl • Motilitatea palpebrala: ochii inchisi: . palparea unor fracturi depresive. disectie de aorta. pneumotorax cu supapa. ampla. encefalopatie hipertensiva). metabolica (uremia) sau vasculara (ASC. tamponada. stari toxice. leziuni ale tegmentului mezencefalo-pontin prin leziuni vasculare sau tumorale. sau lezarea acestei regiuni prin hernie transtentoriala o Respiratie Biot (in salve): este Cheyne-Stokes cu ciclu scurt: respiratii ample alternand cu perioade de apnee. boli renale. profunda. suferinta difuza a emisferelor cerebrale si diencefalului. SLAB • AV: tahicardie: infectii. 40-70/min. soc cardiogen. cu perioada de apnee de durata variabila: disfunctie a centrilor respiratori din regiunea dorso-mediala a bulbului EXAMEN NEUROLOGIC • Semne de iritatie meningiana o Pozitie in “cocos de pusca” o Brudzinski: la flexia capului indoaie genunchii o Redoare de ceafa • Deglutitia: o Pierderea timpului l (de a intindele buzele si a suge apa din lingurita apropiata de buze): leziune la limita superioara a trunchiului cerebral o Pierderea timpului ll ( de a inghiti apa introdusa printre dinti)  Intarziat (tine apa in gura. soc • Hipersudoratia fara febra: leziune in ½ inferioara a bulbului Hipoglicemie Intoxicatie cu anticolinesterazice • Semne de traumatism: plagi ale scalpului. coma hipoglicemica DE OBICEI.• Mirosul: foetor hepatic: insuficienta hepatica Acetone: diabet Alcool: coma alcoolica Amoniac: coma uremica • TA: crescuta: encefalopatie hipertensiva. apoi o inghite): leziune la nivelul nucleului n lX  Abolit (tine apa in gura. leziuni emisferice difuze o Respiratie Cheyne-Stokes: alternanta de perioade de polipnee neregulata si progresiva cu perioade de apnee de 15-30 sec. apare in acidoza metabolica. poate anunta o hernie transtentoriala o Respiratia Kussmaul: hiperpnee sustinuta. COMA VASCULARA scazuta: coma acido-cetozica. NEREGULAT.

o Ochii inchisi: dupa ridicarea pleopelor ele tind sa se inchida rpid: come usoare Dupa ridicarea pleoapelor. ele tind sa se inchida lent si progresiv: come profunde rezistenta crescuta la ridicrea pleoapelor: blefarospasm reflex activitate psihogena inchiderea incomplete a ochilor: leziuni n Vll afectare punte o Clipit spontan: present: integritatea SRA din trunchi Absent: lezarea SRA din trunchi o Clipit reflex: la amenintare: integritate corticala La stimul luminos: integritatea corpului geniculat lateral La stimul acustic: integritate pontina inferioara Lipsa clipitului la stimul lminos sau acustic: leziune de trunchi cerebral .

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reabsorption by kidney Respiratory alkalosis Decrease in Pa CO3 Decrease in plasma Alkaline titration of [HCO3 ] tissue buffers.increased muscle tone/hyperreflexia • • • • • • • .The Four Primary Acid-Base Disturbances Type of Disturbance Primary Alteration Secondary Response Mechanism of Secondary Response Metabolic acidosis Decrease in plasma Decrease in Pa CO3 Hyperventilation [HCO3-] Metabolic alkalosis Increase in plasma Increase in PaCO3 Hypoventilation [HCO3-] Respiratory acidosis Increase in PaCO3 Increase in plasma Acid titration of [HCO3-] tissue buffers. transient suppression of acid excretion and sustained reduction in bicarbonate reabsorption by kidney Multi-focal disorders (with no neuro-imaging signatures) that may mimic a metabolic coma • • • • • • • • • hypertensive encephalopathy DIC endocarditis sepsis thrombotic thrombocytopenic purpura (TTP) fat emboli syndrome diffuse small vessel vasculitis pancreatic encephalopathy superior saggital sinus thrombosis meningitis encephalitis malaria neuroleptic malignant syndrome serotonin syndrome thyroid storm malignant hyperthermia Conditions causing coma + fever +/. transient increase in acid excretion and sustained enhancement of HCO3.

phencyclidine. amphetamines anticholinergic poisoning delirium tremens sepsis DIC leukemia with sepsis infection or hemorrhage caused by myelosuppression thrombotic thrombocytopenic purpura eclampsia (HELLP syndrome) alcoholism . isopropyl alcohol. barbiturates and other sedatives tricyclics and other antidepressants phenothiazines and butyrophenones cocaine. ethylene glycol hydrocarbons cyanide or carbon monoxide poisoning hyperglycemia (DKA and hyperosmolar coma) hypoglycemia Conditions causing coma + thrombocytopenia • • • • • • • Conditions causing coma in pregnancy or the puerperium • • • • • • • • Some toxic and metabolic causes of coma • • • • • • • • • • • • Some toxic and metabolic causes of coma • opiates . phencyclidine gamma hydroxybutyrate salicylates ethyl alcohol. AVM. methanol.portocaval shunt and hypersplenism ischemic stroke pituatry apoplexy cerebral venous sinus thrombosis ICH (aneursym. amphetamines. pre-eclampsia-eclampsia) hypertensive encephalopathy carbamoyltransferase deficiency carrier state (hyperammonemia and hyperglutinemia) porphyria migranous infarct opiates benzodiazepines. cocaine.• • • • • • heat stroke pheochromocytoma porphyria stimulant drug toxicity eg.

hyperammonemia hypoadrenalism porphyria hypoxia hypercarbia hereditary metabolic disorders (carbamoyltransferase deficiency carrier state) Clinical clues suggesting some causes of metabolic coma that may not be readily detected by routine metabolic screening tests Clinical condition Methemoglobinemia • • • • • Clinical clues cyanosis unresponsive to oxygen therapy slate-gray skin color disproportionate tachycardia and tachypnea low pulse oximetry + high PaO2 + normal calculated oxygen saturation chocolate-brown blood .• • • • • • • • • • • • • • • • • • • • • benzodiazepines. dapsone. phencyclidine gamma hydroxybutyrate salicylates ethyl alcohol. coarse. or inhalant abuse in adolescents. narcotics. phenazopyridine. or systemic acidosis from infectious diarrhea due to nitrite-forming bacteria in infants < 6 months more common during the winter months antecedent precipitating illness (CHF. pneumonia) or drugs (sedatives.well water). aniline. naphthalene. chlorates. barbiturates and other sedatives tricyclics and other antidepressants phenothiazines and butyrophenones cocaine. methanol.hypotension bradypnea + alveolar hypoventilation dry. amphetamines. ethylene glycol hydrocarbons cyanide or carbon monoxide poisoning hyperglycemia (DKA and hyperosmolar coma) hypoglycemia myxedema apathetic thyroid storm hyponatremia hypercalcemia hepatic failure. nitroalkanes in nail-poish remover.does not turn red when exposed to oxygen exposure history:.teething gels. benzocaine . isopropyl alcohol. lithium or amiodarone) or discontinued thyroid medication hypothermia without shivering bradycardia +/. increased nitrates .skin or po exposure to oxidising agents (eg. scaly skin • Myxedema coma • • • • • • .

interacts Disoriented Confused speech. unintelligble sounds restless. agitated. disoriented. hypercholesterolemia. unaware No response No response Alert and oriented Coos. nonsensical inconsolable. social. babbles Irritable cry Cries to pain Moans to pain No response Follows commands Localises pain Movement or withdrawal to pain Decorticate flexion Decebrate extension No response Normal. spontaneous movements Withdraws to touch Withdraws to pain Decorticate flexion Decerebrate extension No response A suggested sequence of medical therapy for increased intracranial pressure . distended abdomen (paralytic ileus) delayed "hung-up" DTR's associated hyponatremia. increased serum LDH and CK Appendix Glasgow coma scale for all age groups 4 years to adult Eye opening 4 3 2 1 Verbal response 5 4 3 2 1 Motor response 6 5 4 3 2 1 Child < 4 years Infant Spontaneous To speech To pain No response Spontaneous To speech To pain No response Spontaneous To speech To pain No response Oriented. spontaneous movements Localises pain Withdraws to pain Decorticate flexion Decerebrate extension No response Normal. conversation consolable.• • • • • • • • carotenemic pallor brittle nails puffy face and eyelid edema macroglossia thyroidectomy scar or thyromegaly quiet. speaks. aware Speaking but Inappropriate words. unaware Moans or Incomprehensible. anemia.

a "good" doctor-patient relationship must be fastidiously maintained and the patient should be gently coaxed into a state of full consciousness Clinical features suggesting psychogenic coma (feigned coma) • • • • • • • • • • • • • .if mean arterial blood pressure > 150 mmHg to lower the mean blood pressure to < 140 mmHg IV phenylephrine .1. or the eyes always look towards the ground the eyes are continuously rolled back into the head. Q tip stuck up the nose) should not be used to induce responsiveness . reactive pupils + conjugate eye movements rapid nystagmoid eye movements away from the irrigated earcanal occur during caloric testing of the oculo-vestibular reflex (or sudden patient arousal from coma as a result of caloric testing .• • • • • • • • elevate the head of the bed 30 degrees and maintain the neck in a neutral position emergent ET intubation and manual/mechanical hyperventilation to a PaCO2 of 30 .if mean arterial blood pressure < 90 mmHg +/.5cc/kg of 23.2 mug/kg boluses prn .5 .converged equal. the eyes are conjugately deviated downwards +/. ammonia capsule held under the nostrils.IV normal saline fluid boluses prn to ensure euvolemia 0.35 mmHg IV mannitol . or the eyes always look to the side away from the examiner.4% sodium chloride over 15 minutes IV can be used as last resort if the above measures fail dexamethasone .0.0g/kg over 5 .5 g/kg IV boluses prn .testing should therefore be used as a last resort) active resistance or varying resistance to passive motor tone testing. or the hand falls abnormally slowly onto the face no abnormal reflex posturing in response to painful stimuli the patient may occasionally make voluntary movements or change body position in bed provocative maneuvers (eg.1 .10mg .10 minutes IV thiopental . or cogwheeling resistance with sudden "giving-away" phenomena the patient's hand always manages to avoid hitting the face when the passively uplifted hand is released directly over the central face. or alternatively.if tumor or abscess present pentobarbital infusion or surgical decompression therapy based on the CT scan results active resistance to passive opening of the eyelids a tendency for the eyelids to close abruptly and completely when the lifted upper eyelid is suddenly released (rather than slowly.0. asymmetrically and incompletely) fluttering of the eyelids when the eyelashes are gently stroked any spontaneous eye movements are rapid and jerking rather than slowly roving the patient actually makes eye contact with the examiner when the eyelids are opened.

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