coma

Approach to Coma

A TOPIC ALWAYS NEEDS TO BE AROUSED

DEFINING COMA"unarousable unresponsiveness"

• Defined coma as a state of unresponsiveness inwhich the patient lies with his eyes closed andcannot be aroused to respond appropriately tostimuli even with vigorous Stimulation

• The patient may grimace in response to painfulstimuli and limbs may demonstrate stereotypedwithdrawal responses, but the patient does notmake localized responses or discrete defensivemovements

COMA IS PROLONGED UNCONSCIOUSNESS

Consciousness

• Perception -Awareness of self and environment ( Sensory System)

• Reaction – Meaningful responsiveness (Motor system)

• Wakefulness – (Sleep wave cycle)

Stages of (un)Consciousness

• The terms stupor, lethargy, and obtundation refer to states between alertness and coma

• An alteration in arousal represents an acute, life threatening emergency, requiring prompt intervention for preservation of life and brain function

Coma Pathophysiology

• Coma implies dysfunction of:

– Ascending Reticular Activating System or

– Both hemi-cortices

• Anatomically, this means

– central brainstem structures (bilaterally) from caudal medulla to rostral midbrain

– both hemispheres

Coma - Aetiology

Metabolic:-

– Ischemic hypoxic

– Hypoglycaemic

– Organ failure

– Electrolyte disturbance

– Toxic

Structural:-

– Supratentorial bilateral

– Unilateral large lesion with transtentorial herniation

– Infratentorial

ASSESSMENT OF COMA

Assessment of coma

• Coma is an acute, life threatening situation. Evaluation must be swift, comprehensive, and undertaken while urgent steps are taken to minimize further neurological damage

• Emergency management should include:

• Resuscitation with support of cardiovascular and respiratory system

• Correction of immediate metabolic upset, notably control of blood glucose and thiamine if indicated; control of seizures and body temperature; any specific treatments—for example, naloxone for opiate overdose

• History—through friend, family or emergency medical personnel

• General physical examination

• Neurological assessment—to define the nature of coma

•where is the lesion responsible for coma?

•what is its nature?

•what is it doing?

• Neurological diagnosis is based on history, thoughtful examination, and the appropriate choice of investigations

• This is essential, as there is little point in performing a cranial computed tomographic(CT) scan in a patient in hypoglycaemic coma where urgent correction of the metabolic disorder is paramount and any delay—for example, waiting for a scan—is unacceptable

• The approach to clinical evaluation is used to categorise coma into:

• Coma without focal signs or meningism. This is the most common form of coma and results from anoxic-ischaemic, metabolic, toxic, and drug induced insults, infections, and post ictal states

• Coma without focal signs with meningism. This results from subarachnoid haemorrhage, meningitis, and meningoencephalitis

• Coma with focal signs. This results from intracranial haemorrhage, infarction, tumour or abscess

Keep in mind

• Multifocal structural pathology, such as venous sinus thrombosis, bilateral subdural haematomas, vasculitis or meningitis, can present with coma without focal signs or meningism and so mimic toxic or metabolic pathologies

• Conversely, any toxic/metabolic cause for coma may be associated with focal findings—for example, hypoglycaemic or hepatic encephalopathy

• Also focal signs may be the consequence of pre-existing structural disease; in the septicaemic patient with a previous lacunar infarct, for example, the focal neurology may be mistakenly accepted as signs of the current illness

EXAMINATION

Circulation

• Kocher-Cushing response -

– rise in BP->bradycardia due to rise in ICP -> compression of floor of the iv ventricle fall in BP and tachycardia usually terminal event due to medullary failure

Breathing

• Forebrain– Post hyperventilation

apnea

– Cheyne stoke respiration

• Hypothalamus midbrain– Central neurogenic

hyperventilation

• Basis pontis– Pseudobulbar paralysis

of voluntary center

• Lower pontine tegmentum– Apneustic breathing

– Cluster breathing

– Short cycle periodic breathing

– Ataxic breathing

• Medulla– Ataxic breathing

– Slow regular respiration

– Gasping

NEUROLOGIC EXAMINATION

Level of consciousness

• Arousability is assessed by noise (eg, shouting in the ear) and somatosensory stimulation

• Pressing on the supraorbital nerve (medial aspect of the supraorbital ridge) or the angle of the jaw, or squeezing the trapezius, may have a higher yield than the more commonly used sternal rub and nailed pressure

• Important responses include vocalization, eye opening, and limb movement

Cranial Nerve Exam

• Systematic assessment of brainstem function via reflexes

• Cranial Nerve Exam

– Pupillary light response (CN 2-3)

– Oculocephalic/calorics (CN 3,4,6,8)

– Corneal reflex (CN 5,7)

– Gag reflex (CN 9,10)

Pupils: Key points

• Size dependent on sympathetic and parasympathetic input

• Anatomically near the RAS

• Resistant to metabolic influences

• Small and reactive with metabolic causes

• Unilateral dilation indicates uncal herniation

Pupil

AtropineOpiate

Organophosphorus

Pupil

• Diencephalic (metabolic) Small reactive

• Midbrain tectal Midsize,fixed

• Midbrain nuclear Irregular pear shaped

• 3rd nerve Fixed widely dilated

• Pontine Pinpoint reactive

• Opiate Pinpoint

• Organophosphorus Small

• Atropine Wide dilated

• Lesions above the thalamus and below the

pons preserve pupillary reactions

Eye movements: Exam

• Position at rest– Straight ahead

– Dysconjugate

– Conjugate deviation

• Oculocephalic reflex– Positive “Doll’s eyes”

– Negative “Doll’s eyes”

• Oculovestibular reflex– Cold calorics

• Resting position– Midline

• Deviation suggests frontal/pontine damage

– Conjugate• Dysconjugance suggests

CN abn.

– Moving• Roving, dipping, bobbing

Eye movement

• Metabolic – Roving eye movement,

– Oculocephalic,

– Vestibuloocular

• Supratentorial – Contralateral conjugate palsy

• Thalamus– Upper turn down

Eye movements in Coma

• Midbrain

– Ipsilateral 3rd

• Pontine

– Ipsilateral 6th

– Ipsilateral gaze palsy

– One and half syndrome

– Bilateral gaze palsy

– Ocular bobbing

– Mlf syndrome

Oculocephalic and caloric response

This reflex is usually suppressed (and

therefore not tested) in conscious

patients

If nystagmus occurs, the patient is

awake and not truly in coma; this can

be a useful confirmatory test for

psychogenic unresponsiveness

Corneal reflex

The reflex can be suppressed acutely contralateral to a large, acute

cerebral lesion, and also with intrinsic brainstem lesions. Loss of the

corneal reflex is also an index of the depth of metabolic or toxic coma;

bilaterally brisk corneal reflexes suggest the patient is only mildly

narcotized. Absent corneal reflexes 24 hours after cardiac arrest is

usually, but not invariably, an indication of poor prognosis (assuming

the patient has not been sedated). Corneal reflexes may also be

reduced or absent at baseline in elderly or diabetic patients

Motor examination

• Muscle tone, spontaneous and elicited movements and reflexes

• Asymmetries of these often indicate a hemiplegiaof the non-moving side, implying a lesion affecting the opposite cerebral hemisphere or upper brainstem

• Purposeful movements include crossing the midline, approaching the stimulus, pushing the examiner's hand away or actively withdrawing from the stimulus

• Decorticate posturing consists of upper-extremityadduction and flexion at the elbows, wrists, andfingers, together with lower-extremity extension,which includes extension and adduction at the hip,extension at the knee, and plantar flexion andinversion at the ankle . This occurs withdysfunction at the cerebral cortical level or belowand may reflect a "release" of other spinalpathways

• Decerebrate posturing consists of upper-extremityextension, adduction, and pronation together withlower-extremity extension and traditionally impliesdysfunction below the red nucleus, allowing thevestibulospinal tract to predominate

Motor response to pain.(A) Left hemisphere lesion. The

two figures illustrate localisation of

pain with the left hand and flexion

(left hand figure) or extension (right

hand figure) on the right

(B) Subcortical: unilateral left sided lesion exerting a variable contralateral effect. The figures illustrate flexion to pain with the left hand with either extension (right hand figure) or flexion with the right and hyperextension in both lower limbs

(C) Midbrain upper pontine: a bilateral upper and lower limb extension response

(D) Lower pontine/medullary: a bilateral extensor upper limb posture with either flaccidity or minimal diminished flexor response in lower limbs

ECG changes in coma

(SAH, ICH, INFARCT)

– Tall T, prolonged QT

– Q wave with st depression

– SVT, AF, AFL

– Sinus bradycardia,arrest, nodal rhythm

– A-V block or dissociation

– PVc's, VFL, VF

Case 1

• 24Yrs laborer presented to the hospital with H/O

fall down from height. Admitted the patient in

ER. On the time of admission in ER patient was

unconscious and agitated, GCS 3/15.

– BP= 120/70 mmHg

– PR=110 bpm

– RR= 20 mts

– Temp=37.4 ⁰C

– SPO²= 98%

CT done

Diagnosis

Sub Arachnoid Hemorrhage

Case 2

62 years old male admitted to ED of KAUH on 13

May, 2009. Confusion since today morning,

disorientation, lethargy, abdominal pain,

constipation.

Past medical history: DM ( on OHG agent),

CLD(LC, Hematemesis), HCV, HBV, Portal

hypertension, post splenectomy, esophagitis.

Family history: No family history of similar

condition.

Examination:

o General condition: Disorientation & Confusion

o Skin: No jaundice, no skin rash

o CVS: S1 + S2 + 0

o CNS: Normal reflexes, flapping tremors

o Chest: Bilateral basal crepitation

o Abdomen: Distended, soft, lax, hepatomegally, mild ascitits

Vital signs:RR: 22 BP: 135/78 Pulse: 75 bpm Temp: 36.22º C

Lab:Na: 144 mmol/L K: 4.1 mmol/L Bilirubin: 7 umlo/L Cr: 100 umol/LGlucose: 12.1 mmol/L CK: 2468 IU/LAlbumin: 22 g/L ALT: 69 U/LAST: 110 U/L GGT: 92 U/L Troponin-I 1.6 ug/l

MRI

Diagnosis

Hepatic encephalopathy

Case 3• 64/F, no significant past medical history.

• Elective L/S BTL 0900. During the surgery, D5 at125 cc/ hr.

• Pt in ICU. “Too sedated to go home.” Got IVmeperidine. No PO intake, IV D5 continued.

• 2:45 AM next day, pt. C/O headache, verbal orderfor Tylenol #3.

• At 9:00 AM, nurse tells surgeon of a sodium of127 mEq/L. No new orders, IV fluids werecontinued. At 1:30 pm, pt. lethargic and painmedications, pain meds held.

• At 3:30 pm, she had seizures and respiratory

failure. Neurology call given for seizures. The

patient intubated and ventilated. Repeat of

Serum sodium 122 mEq/L.

Diagnosis

Hyponatremia

SOME MORE IMAGES

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