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ohontrast CT, as soon asthe patients stabilized 8 4 ‘peaswement of ICP © Sometimes . + diagnosis isunclear: lumbar puncture oF EEG Le CSF rramnalion ly oll cele eho abrous ectoxs ination) 4, 9 ON, ct cidolules, Ugh ut, nd ele Bc + Sep'y toad illeuss 1X of underlying drsotden Hf erdclyag sen rage 2065dice: Aidvnond_Agilabin Secabiou seals ( RASS, Y Asseres how aptlajed oe sedated vx Mx f + [Glasgow comascaie) > Noewe® Scofes AS © EvBopening (I: Spontaneous &/ To speech3/ To pain2/ No response 1 © Mototresponse (Ml Obeys6 /LocaliesS/ Withdraws 4 / Flexion 3 / Extension 2 /No response 1 © Verbal response (Vi: Orientated 5 / Confused conversation 4 / Inappropriate words 3/Incomprehensible sounds ° ° ° 2/Noresponse 1 2 /25\s% ocoluaciiso’ © nero = sieabinle gles doweyt to pp bat “Hlertness welche © Be “Merbal stimulus stimulation > decors stimulation ih r le timulat (awe ie fe) > Avise Addurle d 3 plnod wl Sixcssorsve dx “ou He chogh Jong: D indaleglrion T "Lower] poss § Gee, deco foul) Corderosw) > Aous odducled @ srleuded ~ | ponaed nag suf glavton Pai i" ecod fiupons, le eats, lags © to 4 ve both coah'c ws ple artendod & mle Faroe ¢ Telsen o. [omaesic VALUATION) © Taking a compl prior events is critical elf bout the time course forthe chanep Jn mental satusapd shout posible causes (ee, recent travel, ingestion of unusual meals, exposure to possible infections, drug or alcohol use possible trauma} © Head trauma; periorbital eechymosis (raccoon eyes), ecchymosis behind the ear (Bate sig), hemotympanu, SF thinorthea and otorrhes © Hypothermia Environmental exposure, near-drowning, sedative overdose, or Wemicke encephalopathy © Hyperthermia; Heatstroke ‘© ewes, etechial or purpuric ash, hypotension, or severe extremity infections (eg gangrene of one or more toe) Sepsis or CNSinfection Nectle marks: Orug overdose (eg, of opis or insulin) ‘bitten tongue: Seizure © Breath oir: Alcohol, other drug intoxication or diabetic ketoacidosis + srolgi xanaio) should focus onthe flowing © @LeveLof consciousness (6C3) ‘o@éve examinations (detailed below) + Puplaryresponses, + pupils + GERBER « poo's, chao fo HNhng? moans, eo-04 siophtalne + ash > popilloedena, ahival baw ouhoye + Other neuro-ophthalmic reflexes ‘o@ Matar function (eg, fscicity, hemiparesis, asters, multifocal myoclonus, decortcate or decerebrate posturing) co(itbaep tendon cefiees (Asymmetry of tendon refexes and plantar responses: both plantas are often oygeer locce npr Cah tin midbrain on ute fondo dy ‘Bah on wad oes st048)-+ oflen owed ty gape "Dilatation of one pupil: CNL compression -> neurosurgical emergency + Homers syndrome (ptosis + miosis: hypothalamic damage + lateral mid-point act pupils (Le, normal pupils): metabll comes + Bilateral ihtfixed Gated aus one ofthe rai deat ca * Bilateral pinpoint, lighted pups: pontine nury = Bilstewal vnidgestthoo Vegeta ce silly dialed tight fired pupils s BS injun Pageaof5Dieter id-postiontightine-orsightpclted ightined pupils 8S hy © Extraocular movements Oculomotor paresis [Nbsence of blinking in response to visual threat Nystagmus Exophthalmus or enophthalmus Point of interest: ‘* fa patient isin true coma and you lft théir eyelids and let ther go, they wil gradually cover the eyes ‘= Ifa patient isin a hysterical coma and you lift their eyelids, the lids wil rapidly close © Fundi: look for papilloedema and retinal haemorthagé ro-ophthalmic reflexes Oculocephati refiex ‘+ Itis tested by the doll's-eye maneuver ‘+ The eyes are observed while the head is passively rotated from side to side or flexed and extended. + spine injures need to be ruled out before the maneuver is done! + Oculovestibuiar pathways in the brain stem are intact (= reflex is present): eyes move in the opposite direction of head rotation flexion, or extension Oculovestibuiar (cold cori) testing + Indication: f the patient is unconscious and the aculocephalic reflex is absent or the neck i immobilined ‘© First confirm tympanic membrane integrity -> elevate patients head 30° - irrigate the external auditory canal with 50 mL of ice water over a 30-sec period ‘© Nystagmus away from the Irigated + both eyes deviate toward the irigated ear - Intact brainstem ‘+ Respiratory patterns © Periodic cycling of breathing (Cheyne-Stokes or Biot respiration) may indicate dysfunction of both hemispheres or of the diencephalon (BS is intact) (© Hyperventiation (central neurogenic hyperventilation) with respiratory rates of > 40 breaths/min may indicate ‘midbrain or upper pontine dysfunction ‘© An inspiratory gasp with respiratory pauses of about 3 sec after full inspiration (apneustic breathing) typically Indicates pontine or medullary lesions; this type of breathing often progresses to respiratory arrest (© Cushing flex: hypertension + bradycardia + irregular breathing -> ICP ‘© Investigations © Blood and urine Drugs screen (ex: salicylates, diazepam, narcotics, etc) Biochemistry urea, electrolytes, glucose, calcium, etc} Metabolic and endocrine studies Blood cultures (© Imaging -> CT or MRI ©/ CSF examination é eG Page 4of5‘toe Definition: A condition of complete unawareness of the self and the environment accompanied by sleep-wake ston. disoicdeas cycles with > Yawake but not aware" + Follows comatose state © Cause: ifVePibl Wate TO OFLERend hemispheres BLT intact brainstem function eres BUT aie alate function, With complete or partial preservation of hypothalamic and brainstem autonomic function © Prognosis: average life expectancy is 2-5 years ee Pec fe, cohneal «flew + bag wfloy & Ayroe tee + Braiaeaiy otto flies Seeseubatae oO tir Ot spdnlontaus bse! eg? a flea. © There's no clincal evidence of bain function upon physical examination [00 response to poin and no rari nerve reflexes) «© GRRTRGABERY - ceretromeduospinalccomection ©The patents aware but cannot move or communicate verboly de to complete paralysis of neat voluntary inthe ae theeves. © Cause: ‘THE DIFFERENCE BETWEEN COMA AND SLEEP, ‘¢ Sleeping persons respond to unaccustomed stimull Sleeping persons are capable of mental activity (dreams) + Sleeping persons can be roused to normal consciousness + Cerebral oxygen uptake does not decrease during sleep as it often does in coma K. MawaGMeNT + Immeckate stabization (ABC) + frequent monitoring of vital functions + supportive measures, including, when necessary, control of ICP + Admission to an icu + Treatment of underlying disorder + [longterm ese) © [ Skincare} turning to avoid pressure sores and pressure palsies), removal of jewellery (© [Oral hygiene} mouthwashes, suction Eyecare: prevention of corneal damage (is taping, rigation co [fluids intragastric ov Caloriesiguid diethrough afin intraga Sphincters{eathet tube, 3000 keal dally ionvhen essential use Paul's tubing if possible); rectal evacuation PTosl Aecavens | o | Recovery NCS. € 5 F Neoe lave clate foruronout NCS | ‘ { fea tain |_, an ¢ \s oe nly 1 pemounnt Verstanye stale wg “E LeSnain ctoat ln FHCS = mintucally cowrclous qd Pages of,© DEFINITION: a svionme son NE) 4. Diabetic ‘© Hipetelveemias hyperosmolar non-ketotie coma; Ketoacidosis 2. on imbalance: natremias,calcemias 3. Renal failure: uremic encephalopathy Vines as verte See ee (© Hepatic encephalopathy ~ Srociomntsiny: (© Wernicke encephalopathy + Bealyler. 48 NA, 2nd ‘© Thyroid storm (hyperthyroid) + Gndocatnt invec we) ae © Aen esis (hyposdrenal) gestae 6, AG imbalance: hypoxla, hypercapnia, severe acidosis = Taxi egy ‘Laren 7 Toxesopy*poeing + cs, ps Hoot gnss ppt @ HYPOGLYCEMIC COMA Pathogenesis: glucose in blood ~ inadequate supply of glucose to the brain -> neurogiycopenia ‘Acute compensatory mechanisms: reduction of insulinsecretion to undetectable levels, and release ‘of glucagon, adrenaline (SS) Prolonged hypoglycemia compensation: ketogenesis Etiology: o> Drugs’ © Sepsis 04 Acute verfallure 1 pucortoeusa’s £ ala cogen shore > Acute ler fallure cone ayes ) omas, LG-1 secreting tumours TANS. + pallee * tnagpioptiol = pepression, aleahol or drug use © Investigations = Linsulin & J C-peptide: alcoho), adrenocortical failure, critically il + Tinsuling J Creptide: excessive insulin injection Cenogtirous souece’) + insulin & 7 C-peptide: insulin secreting tumouss,sufonylureas_ (ev ogenoUe Soueca > © Management 1 AGC. 4 “a Unconscious patient: IV glucose or 20% dextrose + glucagon. ‘Full meal as soon as mental status permits Conscious glucose PO ‘tnx sugae packs, coca coo Page of?DIABETIC COMAS -3 Yor 944.01 128+ PYaleeric +41, SEVERE DIABETIC HYPOGLYCEMIA (insulin overdose) 2, DIABETIC KETOACIDOSIS Ethiology ‘+ "manifestation in an undiagnosed patient ‘Triggers on the diabetic pationt: major trauma/stre: lure of compliance; infection; ischemia Pathogenesis + insulin > 4 uptake of glucose into cells > hyperglycemia + 4 counterregulatory hormones (glucagon, cortisol, catecholamines, GH) -> unrestricted hepatic ‘ucose production > hyperglycemia + Hyperglycemia > osmoti diuresis > dehydration and electrolyte disturbance * Dehydration + hypovolemia > hypoperfusion > * lactic acid > metabolic acidosis * Without treatment: unconsciousness, from a combination of severe hyperglycemia, dehydration, shock, and exhaustion Clinical features ‘+ From hyperglycemia: polyuria, polipsia, weightloss, muscle pain & weakness + From dehydration: severe abdominal pain, gradual drowsiness = From ketoacidosis: nausea, vomiting, fruity odour, Kussmeut’ respiration * lf severe: LOC, coma Diagnosis: Arterial blood pl < 7,5 + Serum HCO3 < 15+ Ketonurla ‘Management 0. Immediate resuscitation and emergency measures if patient is stuporous or comatose 4 Replace fud losses: IV isotonic ud (0.9% saline + 20 mmol/L KCL) ‘Slowly administered to avoid cerebral edema 2.Continuous infusion of short-acting insulin = Critical to resolve acidosis, not hyperglycemia = Use only regular insulin = Check serum glucose hourly > fit falls below 200 before acidosis is corrected, add glucose to infusion 3 Potassium replacement + As acidosis is corrected, hypokalemia may develop (insulin promotes K+ Into the cels) + When K 3.55.5 mmol/L add KCUK,PO, to fluid to keep Kin the range 4. carbonate therapy: Only given if pH <7.0[otherwis, there's risk of metabolic alkalosis) ‘+3. HYPEROSMOLAR NON-KETOTIC COMA, In Type 2 dehydrated DM Pathogenesis ‘+ Basal insulin is enough to suppress lipoprotein lipase activity > no ketogenesis "+ Relative insulin deficiency decreases glucose utilization while inducing hepatic glucose production Trigger: dehydration caused by excess diuretics, renal fare, burns, sepsis, drugs (glucocorticoids) = Volume contraction -> shift of fluid from neurons to ECF -> mental obtundation and coma Complications: occlusive events (Ml, stroke, arterial insufficiency) Management * 0. 1mmediate resuscitation and emergency measures i patients stuporaus or comatose 1. F 099% saline Iv, aver 48h) ‘+ 2.Search for precipitating event + A.Rehydration +3. Insulin therapy: ‘© Wait ah before starting Page2 of 7Use only regular insulin Initially load, then maintain with a lower dose © Ingeneral lower insulin requirement compared to DKA * Prevouty (SSE + Untreated patient orfion-compliance) + (SRR urge, infection, trauma ose of corticosteroid when undergoing any stressful event : © Presentation’ nausea, vomiting, headache, irritability, letharey seizures, coma, or even death ‘When hyponatremia is accompanied by disturbances in total body Na content, signs of ECF volume depletion or overload also occur CChronie = asymptomatic ‘Management: ‘+ Asymptomatic: slow Nat Infusion of maximally <12mmolin the frst 24h ‘+ Symptomatic: 3% saline IV immediately at a rate of 1 mmol/L per hour until neurologic symptoms are controlled > followed by a rate of 0.5 mmol/L per hour (© Aaute hypernatremia is caused by an excess of water relative to solute (primary gain in Na* or excess loss 0, water) > ae) Gain _in sodium can result from: hyperaldosteronism, Cushing's syndrome, or excessive hypertonic saline or sodium bicarbonate administration Loss of free water can result from gastrointestinal losses or renal excretion (eg, osmotic diuresis or clabetes insipidus} CE: a major symptom is thirst ‘Acute: cerebral pontine myelinolysis> confusion, neuromuscular excitability, selzures, and coma ‘Management: slow replacement of intravascular volume and free water orally or intravenously (©The magnitude of the potassium gradient across cell membranes determines excitability of nerve and muscle (© Evaluation of serum potassium must consider the effects of changes in serum Ph: when serum pH falls, serum potassium rses because potassium shifts from the cellular to the vascular space; and vice-versa © Hyperkalemia Severe if>7mmol/L ‘most commonly seen in patients with end-stage renal disease CCF: weakness, ascending paralysis, and respiratory failure Management ‘© Shift potassium into cells: Glucose plus insulin, Nebulized albuterol, Calcium chloride + Promote potassium excretion: diuretics, enemas, alysis © Hypokalemia ‘Most common causes: + Gloss (diarrhea, laxatives) + Renal loss (hyperaldosteronism, severe hyperglycemia, potessium-depleting diuretics, carbenicilin, sodium pentcilin, amphotericin B) ‘¢ Intracellular shift alkalosis or arse in pH) ‘+ Malnutrition ‘The myocardium is extremely sensitive to the effects of hypokalemia, particularly if the patient has coronary artery disease ori taking a digitalis derivative Page dof 7