EMERGENCY MEDICINE Should be followed by formal pleural drainage
and +/- thoracotomy when condition stabilised.
BASIC FIRST AID Once pleural cavity is drained, wound can be
Check for a SAFE ENVIRONMENT, then ABCDE… sutured or covered with an occlusive dressing.
Airway Check airway is patent. Open mouth- Check for foreign bodies. Circulation Look for clinical S&S of shock: SHOCCCC…
Immobilise neck if head / neck injury suspected Sinus Tachycardia & SOB
Do not move casualties until skilled help and equipment arrive. Hypotension (when 30% lost)
Passengers ejected from vehicles likely to have serious injuries Oligouria
including to cervical spine Cold
If victim not breathing and no hint of cervical damage, Clammy
hyperextend head. Confused
Breathing CPR? Give oxygen if available. Capillary Refill
Circulation Check pulse. Look for haemorrhages, and control by pressure Insertion of 2x Large Bore Cannulae and X Match.
and elevation (do not use tourniquets as they occlude collateral On reassessment of circulatory state, one of three
circulation tissue destruction). possibilities:
Disability Quick assessment of neurological status. Use "AVPU system" 1) Vital S&S N. Pt lost < 20% blood
in primary survey: A=alert, V=responds to voice, P=responds to 2) Vital S&S Improve, but then . Pt lost > 20% +
pain, U=unresponsive. bleeding!
Exposure EYES- Observe size of pupils, symmetry, and response to light. 3) Vital S&S Do not improve: Pt lost >40% blood or are
+ NOSE AND EARS- Presence of blood or CSF are signs of in shock not caused by hypovolaemia.
Secondary fracture of base of skull. Other 2 signs that suggest this are Disability AVPU / GCS…See Consciousness below.
Survey ‘raccoon’ eyes and haematoma in mastoid region. GLASGOW COMA SCALE
MOUTH- Check for blisters, burns, or spots (Sign of poisoning). MOTOR (The M6 Motorway) Learn the Dance…Wave, Point in, Point out,
HEAD- Haematomas and skull asymmetry can indicate Hands up, Hands Down, Fall Over!
presence of fractures. Trauma of skull increases possibility of 6: Request Carrying Out Request
vomiting, with which patient risks compromising their airways. 5: Localises Pain Localising Response.
THORAX- Explore ventilation symmetry and explore their rib Nail-bed with pencil, supraorbital, sternal pressure.
cage to check for possible fractures. 4: Withdraws Pain Pulls limb away.
ABDOMEN- Painful / hard regions can be indication of
3: Flexor Pain Abnormal flexion of limbs (nail-bed pressure).
haemorrhages or organ damage.
PELVIS- Hip pain- Fracture? (May haemorrhage > 1L blood).
2: Extensor Pain Limb extension (adduction, int shoulder rotation,
After examination, and if no signs of bone damage, lie patient down on side to
avoid possible accumulation of secretions / blood in mouth.
During Exposure, also important to get medical details: AMPLE: Allergies,
1: No Response Self Explanatory.
Medication, PMHx, Last Meal, Events leading up to emergency.
VERBAL (V = 5 in Roman)
5: Oriented Who, where, why, year, season, month.
BASIC A&E MANAGEMENT
4: Confused Conversational manner, but some disorientation.
Primary Survey (ABCDE) Secondary Survey Definitive Care
3: Inappropriate Random / exclamatory speech, no conversational .
2: Incomprehensible Moaning. No words.
Airway Assume cervical injury (if suspicion of injury above
clavicles, Hx of high speed impact). 1: None Self Explanatory.
Open mouth: Remove foreign bodies with forceps and EYE OPENING (4 Eyes!)
suction. 4: Spontaneous Self Explanatory.
If vomiting: Turn entire body to side using spinal board (if 3: Speech Any speech / shout. Not necessarily to open eyes.
not in place, tip trolley down by 20o and suction). 2: Pain Pain to limbs as above.
NG tube (unless evidence of skull fracture) / Intubate. 1: None Self Explanatory.
100% O2. Definition of coma: Failure to open eyes in response to verbal command (E2),
Breathing Inspect, Auscultate and Percuss Chest Wall. Immediately life perform no better than weak flexion (M4), and utter only unrecognisable sounds
threatening thoracic conditions: PHOTO!... in response to pain (V2)
TENSION PNEUMOTHORAX Add all together…Severe: 8, Moderate: 9-12, Mild: 13-15.
S&S: RR, mediastinal (& tracheal) shift away Abbreviated coma scale is AVPU: Alert, Voice, Pain, Unresponsive
from affected side, hyper resonance, breath GCS is of no Dx value, but is reliable way of objectively monitoring the clinical
sounds on affected side. course of the patient with an acute cranial insult without elucidating cause.
Tx initially by needle decompression of pleural PAEDIATRIC GCS: For children <2:
cavity at 2nd intercostal space in MCL Pleural 5: Smiles, Listens, Follows
drainage + underwater seal. 4: Cries, Consolable
Simple pneumothorax may Tension when a 3: Inappropriate persistent cry
pt is ventilated Insert prophylactic chest drain 2: Agitated & Restless
prior ventilation. 1: No response
MASSIVE HAEMOTHORAX Exposure Remaining clothes should now be removed. Cover with
Breath sounds, dullness to percussion, Shift of blanket. Do not overheat. AMPLE (See Fist Aid)
mediastinum away from affected side +/- CV SECONDARY SURVEY
instability. HEAD SCALP:
Tx: Pleural drainage and if initial volume of blood Lacerations, Swellings, Depressions.
> 1500mls or bleeding persists at a rate > Exam of occiput will have to wait until pt is turned.
200ml/hr …thoracotomy indicated. Do not probe blindly as may further damage.
Before Dx in ventilated patient, check ET tube NEUROLOGICAL STATE:
is in trachea and not entered right main bronchus GCS, Pupilliary response, Lateralising S&S.
as this may mimic some of the above signs. Hypoxia / Hypovolaemia must be excluded before
Obvious FLAIL CHEST considering intracranial injury.
Part of chest wall is able to move independently BASE OF SKULL: (Line runs from orbit to mastoid process).
to remainder and occurs when ribs are fractured EYES: Raccoon Eyes (bilateral periorbital haematoma),
in at least 2 places. Flail segment falls during Subhyaloid haemorrhage, Scleral Haemorrhage
inspiration as rest of chest rises. Assoc with EARS / NOSE: Haemotympanium, CSF Rhinorrhoea
significant pulmonary contusion hypoxia. If /Otorroea
respiratory failure supervenes despite O2 therapy BATTLE’S SIGN- Bruising over Mastoid Process.
and adequate analgesia (preferably epidural / If CSF mixes with blood and dropped onto sheet, clotting time is
intercostal blockade) …ventilation is required. delayed and double ring pattern displayed. Otoscope exam C/I
CARDIAC TAMPONADE as may Meningitis.
S&S: Becks Triad: JVP (on inspiration- EYES:
Kussmauls’s sign), Muffled HS, BP PEARL. Retinal detachment, Haemorrhages, Foreign
Also: HR, Pulsus Paradoxicus (a 15% in bodies under lids. Simple acuity test. If unconscious,
systolic BP during inspiration), Distended neck corneal reflex.
veins, Confusion. FACE:
Tx: Needle pericardiocentesis. If caused by Palpate. Nasal septal haematoma, loose teeth.
penetrating implement, leave for surgeons. Instability of maxilla IDd with traction on upper incisors.
OPEN CHEST WOUND NECK: With head held firmly by assistant…
Tx: Cover and seal on 3 sides immediately. One Ears: Pinna trauma, external canal, perforation. Check
way valve is formed by flapping motion of free hearing.
edge of dressing prevents air being sucked Bone: Palpation of spinous processes. XR (may still miss
into pleural cavity from outside. 15%)
WILL WESTON Page 1 of 7
THORAX Inspect for bruising, signs of obstruction, asymmetry, Hypo / Hyperglycaemia
wounds. Hypo / (Hypercalcaemia…if severe)
Palpate for crepitus, tenderness, subcutaneous Hypo / (Hypernatraemia…if severe)
emphysema. Hypoxia / Ischaemic brain injury
Potentially life threatening thoracic conditions: Hypoadrenalism
o Pulmonary contusion Renal Failure
o Cardiac contusion Hepatic Failure
o Ruptured diaphragm Respiratory Failure with CO2 retention
o Aortic Tear NEUROLOGICAL
o Oesophageal Rupture Subarachnoid Haemorrhage
o Airway Obstruction Hypertensive encephalopathy
Bruise from diagonal seatbelt may overlay: Encephalitis, Cerebral malaria
Fractured clavicle, thoracic aortic tear, pulmonary BRAINSTEM LESIONS
contusion, pancreatic laceration. Tumour
Mark caused by impact with steering wheel suggests: Haemorrhage, Infarction
Sternal fracture with cardiac contusion. Demyelination, e.g. MS
ABDO GI: Rectal exam, then catheter insertion. Suspect an Trauma
intraabdominal bleed if ribs are fractured (5-11…overlie Wernicke-Korsakoff Syndrome
liver, spleen), marks from seat belt. CORTICAL / CEREBELLAR LESIONS
RENAL: Injury S&S: Flank Pain / Mass / Bruising, Tumour
Haematuria. Haemorrhage, Infarction
PELVIC: Squeezing iliac crest will only ID major injury Abscess
LIMBS Bruising, wounds, deformities. Vascular / Neurological
Palpate all bones, including metacarpal, metatarsal,
Swab any open fractures and cover with sterile dressings.
SPINE Signs of a Spinal Injury:
o BP + Relative HR
o Motor power & sensation below lesion.
o Anal sphincter tone
o Priapism (painful erection of penis)
Taking care if injury suspected, palpate bones and
SOFT Inspect any breach in skin to ascertain site, depth and
TISSUE underlying structural damage.
CONSCIOUSNESS AND COMA
(Neurological Assessment Of Coma: Neurol Neurosurg Psychiatry 2001)
ASSESSMENT OF COMA
DEFINITION: Consciousness- State of awareness of self & environment, Where is the lesion responsible for coma?
determined by 2 separate functions dependant upon separate physiological & What is its nature?
anatomical systems: What is it doing?
AWARENESS (content of consciousness)
Sum of cognitive and affective mental function, dependent on an
intact cerebral cortex. (The absence of all content of
consciousness is the basis for the vegetative state)
AROUSAL (Level of consciousness).
Coma is caused by disordered arousal.
Arousal depends on an intact ascending reticular activating
system and connections with diencephalic structures. Like
awareness, arousal is not an all or nothing concept and
gradations in awareness can be objectively assessed using
measures such as GCS.
Def Profound or deep state of unconsciousness. An individual in a state of
coma is alive but unable to move or respond to his or her
environment. Cf Persistent Vegetative State… See elsewhere.
Path NEUROANATOMICAL BASIS OF COMA
Coma is caused by either or both of
Diffuse bilateral hemisphere damage
Failure of the ascending reticular activating (RA)
The RA system is a core of grey matter continuous caudally
with the reticular intermediate grey lamina of the spinal cord
and rostrally with the subthalamus, hypothalamus, and thalamic Inv Temp Hypothermia
nuclei. It runs in the dorsal part of the brain stem in the Trauma Haematoma, laceration, bruising, CSF / blood in nose /
paramedian tegmental zone. ears, Skull fracture (strep deformity), subcut
A unilateral hemisphere lesion will not result in coma unless emphysema.
there is secondary brain stem compression, caused by Skin: Needle marks, cyanosis, pallor, rashes, turgor
herniation, compromising the ascending RA system. Breath OH, ketosis, uraemia.
Extensive bilateral damage or disturbance of the hemisphere
Heart,Lung Murmurs, rubs, wheeze, creps, consolidation, collapse.
function is required to produce coma.
Abdomen Organomegaly, Ascites, Bruising, Peritonism, Melaena
Bilateral thalamic and hypothalamic lesions also cause coma
Infection Foci: Abscesses, Bites, Middle Ear infection
by interrupting activation of the cortex mediated through these
structures. Meningitis Neck stiffness, rash, focal neurology
In hypothalamic lesions, phenomena associated with sleep, Eyes SHIT! MALE TB
such as yawning, stretching, and sighing, are prominent. UNILATERAL FIXED DILATED PUPIL: Herniation of temporal lobe
The speed of onset, site, and size of a brainstem lesion (coning) through tentorial hiatus & compression of 3rd CN. Surgery!
determine whether it results in coma, so brain stem infarction or BILATERAL FIXED DILATED PUPIL: Cardinal sign of brain death.
haemorrhage often causes coma while other brain stem Also: Deep coma of any cause (esp barbiturate intox / hypothermia)
conditions such as multiple sclerosis or tumour rarely do so. PINPOINT PUPILS: Opiate overdose or pontine lesions (that interrupt
Lesions below the level of the pons do not normally result in sympathetic pathways to dilator muscle of pupil).
coma. Drugs and metabolic disease produce coma by a MIDPOINT PUPILS (that react to light ): Characteristic of coma of
depression of both cortex and ascending RA system function. metabolic origin / CNS depressant drugs.
Cause TOXINS FUNDI: Examine for papilloedema (indicates ICP)
Drug overdose, OH, anaesthetic gases, CO poisoning. MOVEMENTS: LATERAL DEVIATION OF EYES:
METABOLIC: CAN GO FAILURE Look AWAY from paralysed limbs: Ipsilateral cerebral haemorrhage
WILL WESTON Page 2 of 7
/ infarction S&S Individuals in such a state have lost thinking abilities and awareness
Look TOWARDS paralysed limbs: Contralateral pontine lesion of surroundings, but retain non-cognitive function and normal sleep
MOVEMENTS: patterns. Even though those in a PVS lose higher brain functions,
Passive head rotation ocular deviation in opposite direction other key functions such as breathing and circulation remain relatively
(Doll’s head reflex). This normal reflex is lost in v. deep coma and intact. Spontaneous movements may occur, and eyes may open in
absent in brainstem lesions. response to external stimuli.
Caloric response: Normal = Ice cold water external auditory
meatus Eye deviation towards affected side + Nystagmus away. RULES & REGULATIONS SURROUNDING DEATH
Mx ABC of Life Support ENGLISH LAW…
Does not require a doctor to confirm death has occurred or that 'life is
O2, IV Access extinct' …VERIFICATION OF DEATH
Does not require a doctor to view the body of a deceased person
Stabilise Cervical Spine Does not require a doctor to report the fact that death has occurred
Does require the doctor who attended the deceased during the last
Blood Glucose illness to issue a death certificate detailing the cause of
death…CERTIFICATION OF DEATH
Control Seizures Certifying doctor required to enter:
PART 1: Conditions which led directly to death in, so disease /
Consider IV Glucose, Thiamine, Nalaxone, Flumazenil condition which started sequence is in lowest used line.
PART 2: Any other significant conditions which may have
Brief Examination contributed to death.
If the death occurs in the patient's own home then it is wise to visit as
ABG, FBC, U&E, LFTs, ESR, TFTs, Cortisol
soon as the urgent needs of living patients permit.
Ethanol, Toxic Screen, Drug Levels
If the death occurs in a nursing or residential home and the GP who
Blood Cultures, Urine Culture, Malaria
attended the patient during last illness is available, then it is sensible for
GP to attend when practicable and issue a death certificate
If 'on-call' doctor is on duty, unlikely any useful purpose will be served by
Reassess and plan further investigations
that particular doctor attending. In such cases, recommended that GP
ABC of Life Support Airway
advises home to contact undertaker if they wish body to be removed and
ensure GP with whom patient registered is notified as soon as practicable
UNEXPECTED / SUDDEN DEATH
Disability i.e. GCS (Don’t forget Glucose)
If in patient's home, or nursing / residential home, recommended that
there is visit by GP with whom patient is registered, to examine body and
O2, IV Access Hypoxic
confirm death, (although this is not a statutory requirement). GP should
then report patient's death to coroner - Generally through local police.
Stabilise Cervical Spine
In any other circumstances, request to attend is likely to have been
generated by police / ambulance service. Generally wise (Esp for 'on-call'
Blood Glucose Hypo / Hyperglycaemia doctor), to decline to attend and advise services of a retained police
surgeon be obtained by caller.
CONFUSION: See CCC Delirium (Psychiatry)
Thiamine, Glucose THAMINE Lactic acid Enceph-
Nalaxone alopathy(Wernickes),Numbness,Weakness. INTRACRANIAL PRESSURE AND CEREBRAL BLOOD FLOW
Flumazenil: If airway NALAXONE: Opioid antagonist
REMEMBER: CPP = MAP – ICP World Anaesthesia, Oxford.
compromised FLUMAZENIL: Benzodiazepines antagonist
Blood flows to brain via carotid and vertebral arteries Anatomise at COW.
Brief Examination ICP: Intracranial Pressure is pressure within rigid skull.
CPP: Cerebral Perfusion Pressure is pressure driving blood through brain.
MAP: Mean Arterial Pressure is diastolic pressure + one third of pulse
ABG Hypoxaemia, CO
pressure (difference between systolic and diastolic). MAP is thus between
systolic and diastolic pressures, nearer diastolic.
U&E Uraemic Encephalopathy
LFTs Hepatic Encephalopathy Principle constituents within the skull: Brain (80%), Blood (12%) CSF (8%).
ESR Infection v.intracranial (constant) = v.brain + v.CSF + v.blood + v.mass lesion
TFTs, Cortisol Hypothyroidism, Hypoadrenalism If mass lesion / oedematous brain expands some compensation is possible as
Ethanol, Toxic Screen, Drugs OH, Drugs CSF and blood move into spinal canal and extracranial vasculature
Blood C, Urine C, Malaria Septicaemia, Meningitis respectively. Beyond this point, further compensation is impossible
CXR Pneumothorax, Cancer, Infection Dramatic ICP .
Normal CPP is 80 mmHg. If < 50 mmHg there is metabolic evidence of
Reassess and plan further CT (mass lesion, IC haemorrhage) ischaemia and electrical activity. CPP of <70 mmHg gives poor prognosis!
investigations CSF (Only if mass lesion excluded on CT: Normal brain autoregulates its blood flow to regardless of blood pressure by
SA haemorrhage, meningoencephalitis) altering resistance of cerebral blood vessels.
Prog Depends on cause. CAUSES OF ICP: THIN, BB
o CSF Trauma
BRAIN DEATH o Hypoxia (Vasodilation) Hydrocephalus
Def BRAIN DEATH: Irreversible loss of capacity for consciousness, o Hypercapnia (Vasodilation) Infection
combined with irreversible loss of capacity to breathe. o Pain Neoplasia
PRECONDITIONS FOR CONSIDERING BRAIN DEATH DX o Cerebral perfusion pressure. Bleeding
Patient is deeply comatose: I.e. Not due to following… o Exaggerated hypertension. Benign intracranial HT
Drug induced (E.g. narcotics, hypnotics, tranquillisers) S&S OF ICP:
Hypothermia ( Rectal T must > 35oC) o Headache - typical of raised intracranial pressure
Metabolic Conditions: E.g. Electrolytes, Acid Base, Glucose o Vomiting
A disorder that can cause BD has been firmly established (e.g. SAH) and o Confusion and Conscious level.
there is irremediable structural brain damage. o Visual Disturbances:
Pt is maintained on ventilator since spontaneous respiration inadequate. Blurring
TESTS FOR CONFIRMING BRAIN DEATH Obscuration - transient blindness
Pupils fixed and unreactive to light. Papilloedema ( pressure around optic nerve)
Reflexes absent: o Retinal haemorrhages if the rise in ICP has been rapid
Corneal, Gag, Cough (suction catheter in trachea), Doll’s Head, o Cushing's peptic ulceration
Ice Water Calorics o Slowly head size (children)
Spontaneous respiration absent Classic Hx: Conscious level after an insult, followed by improvement then
Pt disconnected from ventilator long enough to allow CO2 to progressive drowsiness. The situation is an acute medical emergency.
above threshold for stimulating respiration (PaCO2 = 6.7kPa) After brain injury, cerebral blood flow may (MAP falls due to escaped
WHO MAY MAKE THE DECISION blood +/or ICP increases due to swelling / lesion size). To prevent
2 Experienced doctors (1 Consult and + 1 SpR or above). Tests usually neuronal death (secondary brain injury), flow of well oxygenated blood must
repeated after 6-24 hrs, before brain death finally confirmed. be restored.
CORTICAL BRAIN DEATH (PVS) CPP may be maintained by MAP or ICP.
Def Cortex destroyed. Often brainstem still intact, e.g. persistent ICP should be controlled when CPP is < 70mmHg +/or ICP > 20mmHg.
vegetative state, i.e. Pt can survive indefinitely if sufficient nutrition. Measures to increase MAP should be instituted prior to starting more complex
Inv To be diagnosed must be demonstration of no perfusion of cortex via methods of ICP control.
cerebral angiography. Not sufficient to just show no EEG activity. MAP CONTROL:
WILL WESTON Page 3 of 7
Control of other sites of haemorrhage has highest priority (with oxygenation). Intracerebral
Further MAP, once normovolaemia is achieved, is usually accomplished Diffuse injuries
with adrenaline, though dopamine may be used. S&S
VENTILATION: Carbon dioxide dilates cerebral blood vessels volume of
blood in intracranial vault ICP. Ventilate to normocapnia.
INTRAVENOUS FLUID THERAPY: Hypertonic solutions and osmotic diuretics Inv /
e.g. Mannitol, water content of brain tissue. Mechanism requires intact
BBB. Mannitol is a fluid and so will of course circulating volume. Mx
POSITIONING: Helps drain CSF…Position with head at no > 30 to horizontal. Prog
Further elevation seems to produce a paradoxical in ICP.
SUBARACHNOID HAEMORRHAGE (SAH)
HEAD INJURY Def Acute condition involving sudden haemorrhage into space b/w
Def arachnoid membrane and pia mater (adjacent to brain).
Christmas Present Analogy…Wrapping Layers: Subarachnoid space contains the cerebrospinal fluid.
Jelly …Brain PP 8/100,000/yr; Typical age: 35-65
Cling film …Arachnoid Aneurysm assoc conditions: connective tissue diseases, AVM,
Paper bag …Dura FHx (SAH:3-5x risk), bact endocarditis.
Cardboard box …Skull Risk Factors for aneurismal rupture: BP, Smoking
Brown paper …Scalp Cause Trauma > intracerebral aneurysms [80% of non traumatic] >
Phys Brain floats within CSF Brain undergoes significant arteriovenous malformations (AVM) [15%], tumour,
translation & deformation when head subjected to forces. perimesencephalic haemorrhage, pituitary apoplexy
Forces that result from either deceleration / acceleration of Path
Common sites of berry aneurysms:
brain can injury by direct mechanical effects or by shear-type
forces on axons. In addition to translational forces, brain can
experience rotational forces, which can shear injuries.
In DECELERATION injury (head impacts stationary
object…windshield) skull stops moving almost instantly, but
brain continues to move within skull toward direction of impact
for a very brief period forces acting on the brain as it
undergoes both translation and deformation.
In ACCELERATION injury (direct blow to head), force applied
to skull causes skull to move away from applied force. Brain
does not move with skull, and skull impacts brain translation
and deformation of the brain.
Intracranial compartment divided into 3 compartments by 2
major dural structures: Falx Cerebri and Tentorium Cerebelli.
TENTORIUM CEREBELLI divides posterior fossa or
infratentorial compartment (the cerebellum and the brainstem)
from supratentorial compartment (cerebral hemispheres). Junctions of:
FALX CEREBRI divides supratentorial compartment into 2 Post comm + int
halves and separates left and right hemispheres of brain. carotid;
Both falx and tentorium have central openings and prominent Ant comm + ant
edges at borders of each of these openings. When a significant cerebral;
in ICP occurs, caused by either a large mass lesion or middl cerebral.
cerebral edema, brain can slide through these openings within 15% are multiple
falx or tentorium, a phenomenon known as herniation. As brain
slides over free dural edges of tentorium or falx, it is frequently
injured by dural edge. Several types of herniation exist:
1) TRANSTENTORIAL HERNIATION occurs when medial S&S Sudden onset of worst ever HEADACHE (> occipital)
aspect of the temporal lobe (uncus) migrates across free edge Nausea +/- Vomiting
of tentorium. This causes pressure on third CN, interrupting Syncope
parasympathetic input to eye and resulting in dilated pupil. This Photophobia
unilateral dilated pupil is classic sign of transtentorial herniation Mental status
and usually (80%) occurs ipsilateral to side of the transtentorial Collapse +/- Seizures Coma
herniation. In addition to pressure on third CN, transtentorial BP
herniation compresses brainstem. Ocular Haemorrhage (Terson syndrome)
2) SUBFALCINE HERNIATION occurs when cingulate gyrus on Neck stiffness (Kernigs +ve [takes 6 hrs to develop]: Each hip
the medial aspect of frontal lobe is displaced across midline is flexed in turn, & then attempt to straighten the knee while
under free edge of falx. This may compromise blood flow keeping the hip flexed = pain)
through anterior cerebral artery complexes (located on medial FOCAL NEUROLOGY
side of each frontal lobe). Subfalcine herniation does not cause DDx Only 25% with sudden severe headache have SAH.
same brainstem effects as caused by transtentorial herniation. Migraine, Meningitis, Intracerebral haemorrhage
3) CENTRAL HERNIATION occurs when diffuse ICP occurs Inv / Hx + Physical Examination
and each of cerebral hemispheres is displaced through Dx CT Non contrast CT of brain (misses 2% of small
tentorium significant pressure on the upper brainstem. bleeds)
4) UPWARD, OR CEREBELLAR, HERNIATION occurs when LP If –ve CT for haematoma / hydrocephalus
either a large mass or pressure in posterior fossa is present Bloody Yellow (Xanthochromia)
and cerebellum is displaced in an upward direction through the RBC count (> 100 000 / mm3)
tentorial opening Significant upper brainstem compression. Angiogrm Cerbral angiogram: Gold Standard
5) TONSILLAR HERNIATION occurs when pressure Mx Bed Rest + BP monitor + CNS re-examine
develops in posterior fossa. In this form of herniation, cerebellar Clip aneurysm to prevent rebleeds
tonsils are displaced in a downward direction through foramen Control severe BP
magnum, compression on lower brainstem and upper Analgesia for headache + bedrest +/- sedation for 4/52
cervical spinal cord as they pass through foramen magnum. Nimodipine (Ca ant): for 2-3/52 if BP allows
PP Comp Rebleeding: cause of death (30% risk in 1 few days)
Cause Vascular spasm: follows bleed ischaemia +/- CNS deficit
Class MECHANISM Prog Mortality Grading
Blunt Trauma: High / Low Velocity Grade Signs Mortality
Penetrating Injury: Stabbing / Shootings / Other foreign bodies I None 0%
SEVERITY II Neck stiff + cranial nerve palsy 11%
Mild: 14-15 III Drowsiness 37%
Moderate: 9-13 IV Drowsiness + Hemiplagia 71%
Severe: 3-8 V Prolonged Coma 100%
Almost all mortal = 1 month. Post 1/12, 90% survive ≥ 1 yr
ACUTE DRUG OVERDOSE / POISONING
S&S Common Drugs: See BNF for more
Fast / Irregular Pulse Salbutamol, Tricyclics
WILL WESTON Page 4 of 7
Coma Benzodiazepines, OH, Opiates, Tricyclics fat.
Pupils Constricted Opiates STRAW Clotting Disorders:
Pupils Dilated Cocaine, Tricyclics Dark Skinned: May mask bruising. UV light needed
Hypoglycaemia Insulin, Alcohol DISAPPEARS Clotting Disorders:
Renal Failure Salicylate, Paracetamol 14-15 days o Haemophilia, Leukaemia and Platelet disorders)
Met Acidosis OH, Paracetamol, CO poisoning (range 1-4 /52) o Some Infections (meningitis)
Inv / History HPC + Psychiatric: Intended action? Previous / Current o Liver Disease ( including alcoholism)
Dx Disorders. Suicide risk? Nb: Pt may not be telling truth. o Vitamin C deficiency
o Poor nutrition
Indexes MIMS, eMIMS, BNF, TICTAC.
Bloods FBC, U&Es (Renal F), Glucose, ABGs, LFTs (Liver F,
ABRASION Portion of body surface from which skin / mucous
Syn: membrane has been crushed or removed by rubbing. A
Tox Check 4 hourly Serum / Urine: Paracetamol and
Scratch, Graze superficial injury, confined to epidermis/dermis. Due to (1)
Salicylate levels (plot on graph) +/- other assays.
Direct impact: imprint (may reflect pattern of causative
Monitor Temp, Pulse, RR, BP, Glucose, Sats, Urine OP, ECG
surface) or (2) Tangential impact: graze or scratch (may
Care Urinary Catheter, ITU if respiration. reflect direction of impact)
Tx ABC LACERATION Full thickness tearing of skin / tissue due to stretching &
Latin: to tear crushing by blunt force. Characteristics: Ragged edge,
Ventilation? Any of below: Associated bruising/abrasion, Tissue bridges
If RR< 8/min Provides little specific information about the causal object.
PaO2 < 8kPa when on 60% O2
INCISION Clean division of full thickness of skin (or other tissue) by
Airway at risk e.g. GCS < 8
Latin: to cut into sharp-edged instrument. Characteristics: Clean cut edges,
No associated bruising/abrasion, No tissue bridges. Incised
wound is LONGER > DEEP. Provides little specific
Unconscious? Nurse semi prone
information about causal object
Investigations: See above PENETRATING Small hole made with a sharp point. DEPTH > LENGTH on
body surface. Due to sharp/flat instrument, e.g. knife
Supportive Measures: (STAB), a sharp/thin, e.g. needle (NEEDLE PUNCTURE) or
Absorption: Consider Gastric Lavage +/- Activated charcoal blunt/long/rigid, e.g. wooden stake (PUNCTURE). Shape
Specific measures: Antidotes. See Oxford HB and size of wound often indicate dimensions of weapon.
NB: NEVER INDUCE VOMITING! THERMAL Application of dry / moist heat :burns & scalds. Cold injury
G Lav INDICATION: ELECTRICAL Heat produced by electrical flow.
Only of use if presentation within 1 hour of poisoning and if FIREARM Small mass, high velocity projectile fired from gun.
potentially toxic dose of drug has been taken.
CONTRAINDICATIED: COMMON SIGNS / SYMPTOMS AFTER AN RTA
Ingestion of petroleum products, corrosives, acids, alkalis, CONTRIBUTORY FACTORS IN CRASHES
bleach, descalers (exception: paraquat). Intoxication Alcohol, Drugs, Carbon Monoxide.
Unconscious / Unable to protect airway (unless intubated) Human factors Reckless, Speeding, Fatigue, Inexperience, Shoes.
PROCEDURE Environmental Fog, Rain, Ice, Snow, Leaves, Sun, Visual Obstruction.
Monitor O2, Suction apparatus to hand, Pt in L Lateral Position Mechanical failure Tyres, Brakes, Steering
Raise foot of bed by 20cm Natural disease Ischaemic Heart Disease, Stroke, Epilepsy.
Pass lub tube (14mm ext diam) via mouth with pt swallow PEDESTRIAN Most vulnerable road user (Esp children / elderly)!
Confirm position of tube: Blow air and auscultate over stomach Dynamics of crash depend on relative heights above ground of impact site and
Siphon contents: Check pH with litmus paper. centre of gravity (COG) of pedestrian.
Perform Lavage: Use 300-600mL tepid water. Massage Left IMPACT BELOW COG throws victim onto bonnet (or roof at > speed).
Hypochondrial area. Victim acquires velocity of vehicle only to be thrown onto road surface by
Repeat until no tablets in siphoned fluid. violent braking.
Leave activated charcoal in stomach unless OH, Fe, Li, IMPACT AT COG shunts victim in direction of travel
Ethylene glycol ingested. IMPACT ABOVE COG throws victim under vehicle
Pull out tube: Occlude end – prevents aspiration of fluid left in.
PRIMARY INJURIES: Due to direct impact of vehicle against victim.
A Chr ACTIVATED CHARCOAL: Car bumper injury to lower leg, if fixed by weight bearing (bruise,
Absorption of drugs from gut with single dose: abrasion, laceration, fracture). Height of injury above heel of shoe is
Salicylates, Paracetamol important. Primary injuries may harbour trace evidence (paint, metal) of
Absorption of drugs from blood with repeated doses: evidential value in 'hit and run' collisions.
Carbemazepine, Dapsone, Theophyllines, Quinine, A high fronted van will hits the thigh.
Digoxin, Phenytoin, Phenobarbitol, Paraquat. Flat fronted lorry or bus hits torso.
Prog SECONDARY INJURIES: Due to impact against bonnet, windscreen, road
surface or other object/vehicle.
FORENSIC MEDICINE: USEFUL FOR A&E!...USEFUL DEFINITIONS Bonnet & windscreen frame may fracture skull or injure chest & abdomen.
WOUND: (legal) Breach of full thickness of skin (or lining of lip). Excludes Thrown Road injures head, chest, abdomen Sliding abrasions,
abrasions, bruises, internal injuries and fractures! lacerations.
WOUND Disruption of continuity of tissues produced by external Running over Flaying lacerations to the limbs.
(medical) mechanical force. Speed of impact cannot be estimated from severity of injuries. Can only
INJURY: Often used synonymously with wound but can have a wider state whether injuries were mild, moderate or severe. Skid marks offer
Latin: injuria (not use, incl damage to tissues by heat, cold, chemicals, only objective evidence of vehicle speed.
the law) electricity, radiation, in addition to mechanical force SPEED OF IMPACT % FATALITIES
LESION: Originally meant injury, now more widely applied to include 19-24 mph 10%
Latin: laesio any area of injury, disease or local degeneration in tissue 24-30 mph 47%
(hurt) causing a change in its function or structure'' 31-36 mph 73%
TRAUMA: Bodily harm with / without structural alterations resulting 50% of fatalities are hit < 30 mph. 50 % serious injured are hit < 21 mph
from interaction with physicochemical agents, imparting VEHICLE OCCUPANTS: Occupants move towards the point of impact.
energy to tissues. May morphologically apparent There are 5 main patterns of impact:
damage (wound) or produce physiological imbalance (eg 1-HEAD ON INTO A STATIONARY OBJECT (Speeds + Impact energy additive)
reflex cardiac arrest by neural stimulation) & 2o effects (eg E.g. Tree, another vehicle ()
thrombosis, infection, obstruction of tubular organs) Driver and front passenger may strike
CLASSIFICATION OF INJURIES Dashboard, windscreen & pillars (skull & brain).
BRUISE Escape of blood from ruptured small vessels into Steering wheel (chest-lacerated lung & heart).
Syn: Contusion, surrounding tissues. Resulting discolouration seen through Parcel Shelf (# knees & pelvis)
Ecchymosis overlying intact skin. Due to blunt force trauma. Pedals trap the ankles
Site, shape, size, severity are very variable. Rear passenger hits seatback or over into front
DARK RED Petechiae- Pin head size bruise < 2mm Deceleration whiplash (flex/extension) neck, DAI brain injury and
Extravasated blood tracks along natural/traumatic planes of ruptured thoracic aorta.
PURPLE < resistance, influenced by gravity & body movement. e.g. 2-REAR IMPACT (Speeds Subtractive)
Blow on temple Bruise on cheek Whiplash (extension/flexion) with no restraint- Seats and head restraints
BROWN Fractured jaw Bruising on neck support torso and neck
Fractured hip Bruise on thigh Risk of petrol fire
GREEN Bruising increased in following: 3-SIDE IMPACT -Direct
4-5 days Infants: Loose, delicate, fatty tissues which bruise Risk of side intrusion
easily. Left: Limb, Spleen, L Kidney, Lung
YELLOW Elderly: Degeneration of vessels & connective tissue. Right: Limb, Liver, R Kidney, Lung
7-10 days Female / Obese: Greater proportion of subcutaneous 4-SIDE SWIPE -Glancing
WILL WESTON Page 5 of 7
-Less risk of side intrusion SUPPLEMENTARY BLOOD TESTS:
5-ROLL OVER -less damaging Grp, XMatch
Rolling spreads time of impact) unless occupant is ejected. LFT's: Jaundice, Malignancy
SEATBELTS: V Effective in mortality / injury in low - medium speed impacts: Clotting: Haemorrhage, Warfarin / Heparin, Liv Disease
Diagonal strap restrains upper torso (prevents impact with steering wheel, Sickle Cell Test: depending on ethnic origin
upper dash) TFT's: Thyroid Disorders
Horizontal strap restrains lower torso and pelvis, (prevents impact with ECG INDICATIONS:
lower dash, parcel shelf) IHD, HT, RhF, Resp Disease: Smoker, Pulm HT
Area of straps spreads deceleration force over a wider area than Recommended for all over 40 or 50 years old.
localised impact Consent (check surgical and verbal anaesthetic)
Stretching of strap fabric increases the time over which deceleration Optimise
forces are spread Premedicate
Prevents ejection through windscreen or burst door
ANXIETY - Depending on needs of patient - Use anxiolytics
HOWEVER…Seat belt injuries are common
PARASYMPATHETIC excretion which is normally enhanced
Bruising across chest & abdomen
by general anaesthetics, e.g. salivary, lacrimal - use
Neck injury and carotid artery rupture anticholinergics, e.g. hyoscine
Fractured sternum, ribs, clavicles AUTONOMIC NERVOUS SYSTEM reflexes, which is
Lacerated mesentery, bowel particularly useful in eye and gonadal surgery
Lumbar spinal injury AMNESIA AND ACTIVE SEDATION - e.g. anxiolytics which
Rarely more damaging than if a seatbelt is not worn. produce orthograde amnesia such as lorazepam, temazepam
Other safety features: ADJUVANTS TO ANAESTHESIA, depending on circumstances:
Airbags Antacids, particularly H2-receptor antagonists
Crumple zones absorb impact energy and increase the duration of impact Antibiotics
Laminated windscreens deform without shattering and prevent ejection Antiemesis
Side impact bars Analgesia
Burstproof door locks to prevent ejection Bronchodilators
Padded steering wheel and collapsable column Steroids, e.g. adrenal insufficiency
Breakable controls and mirrors Local Anaesthetic, e.g. EMLA for siting IV lines
MOTORCYCLIST Transfer to theatre – bed/chair/oxygen etc
High speeds, unstable, no protection, difficult to see. INTRAOP – (AIMS) – HONE
PRIMARY impact injury may be to leg. Haemodynamic stability
SECONDARY impact injury: head, neck, chest and abdominal injury. Optimal fluid management
Helmet and leathers provide the only protection. Normocarbia, Normoglycaemia, Normothermia, Normoxia
Energy must be dissipated by sliding or rolling along the road. Excellent pain control
METHODS – (ANAESTHETIC ROOM) – MISTS, DAM, TIA
Enzyme Inducers: GAP PRICE Enzyme Inhibitors: MC FEED CAKE Tilting trolley
Griesofluvin Metronidazole Skilled assistance
Alchohol (chronic) Ciprofloxacin Drugs
Phenytoin Fluconazole Access
Primidone Erythromycon Monitoring
Rifampicin Ethanol (acute) Transfer to theatre for induction?
Inhalation agents Dextropropoxyphene Induction
Carbamazapine Cimetidine Airway
Ethanol Amiodarone THEATRE – PMR
CAUSES OF NEUTROPHILIA: PAMMI’S BITS Reversal
Pregnancy POSTOP – ABCD, AFTER
Acute haemorrhage Airway
Myeloproliferative disorders Circulation
Iatrogenic – prednisolone Drugs, Disability, DVT (is clexane prescribed)
Severe metabolic disease e.g DKA Analgesia
Bacterial infections Fluids
Inflammatory disesae Temperature
Trauma Endocrine – check blood sugar
Surgery Recovery site – ITU / HDU / recovery
FITNESS FOR ANAESTHESIA Can be adapted e.g for RSI: ‘In place of safety I ensure I have MISTS, DAM’
Fitness classified by American Society of Anesthesiologists (ASA) as follows:
CONDITIONS WHICH REQUIRE SPECIAL ATTENTION / PREPARATION
1. Normal healthy patient ANGINA
2. Mild systemic disease From the history, distance walked before onset
3. Severe systemic disease that limits activity but is not incapacitating Exercise tolerance tests, e.g. Bruce protocol on treadmill
4. Incapacitating systemic disease; threat to life Angina at rest is high risk.
5. moribund patient not expected to survive 24 hours +/- surgery ASTHMA
Presents few problems to anaesthetist if condition well-controlled.
Groups 1 - 3 have No / Little risk with Normal Anaesthesia. Important to note Medication taken at normal doses up to surgery. Only pre-operative
that none of these are an absolute CI to anaesthesia. Instead, they are ways of investigation of note is use of a peak flow meter. Possible postponement
comparing wellbeing of patient with importance of the procedure: Production of or change in medication may be warranted by:
a risk-benefit concept for surgery and anaesthesia. PEFR < 50% of the normal maximum
PEFR less than 200l/minute
HOW DO YOU ANAESTHETISE XYZ?
Significant decrease in the morning PEFR
PREOP – I,E,HEMI,COPT Severe asthmatic usually on a maximal drug regimen before assessment.
Introduction & Tailored dose of steroids may be used e.g. 30-60mg prednisolone once
Explanation of role daily, before and after surgery.
History: Especially: COPD
RED JAM HATS, Existing CardioResp Disease COAD requires intensive preoperative assessment and Tx in order to minimise
PMHx / PSHx: + Dental procedures - caps, bridges or reactions risk of postoperative complications. Assessment includes:
to anaesthetic, any recent general anaesthetic or "awareness" SPUTUM CULTURE: Growth and sensitivity to antibiotics
while under general anaesthesia PEAK FLOW: Before and After bronchodilators to determine whether
Examination…Especially: reversible element of airways obstruction
HT, SOB, LVH, Peripheral oedema, Murmurs, Cough ABGs: to determine hypoxic or hypercapnic drive
Hydration: Skin turgor, Urine OP, Fluid intake, BP, HR. SPIROMETRY: ? Cancel if FVC < 2 L or FEV < 1L or FEV1/FVC i< 0.5
Medications and allergies Subsequently, preoperative antibiotics and physiotherapy are provided.
Investigations Pain relief is particularly important if abdominal surgery is undertaken,
STANDARD BLOOD TESTS: e.g. epidural analgesia may be used to permit the patient to cough.
U&Es, Hb, Hct, FBC, Glucose DIABETES
WILL WESTON Page 6 of 7
ELECTIVE Sx: IDDM
Admit >24 hrs before surgery
Begin / Continue a bd regimen of medium & short acting insulin
On day of surgery commence i.v. Glucose and Insulin therapy
ELECTIVE Sx: NIDDM
stop oral agents on morning of operation
If fasting blood [glucose] < 7.0 mM then no action required
If fasting blood [glucose] > 11 mM, or operation prolonged, then
IV glucose and insulin therapy indicated
EMERGENCY Sx: IDDM / NIDDM
All admitted for emergency surgery require IV control of blood
glucose irrespective of severity of their diabetes.
If patient is in DKA crisis, effective control of metabolic disorder
will be advantageous in two ways:
Vomiting and abdominal pain will be relieved; these
may have been original indications for surgery
Surgery will be safer
A few hours spent correcting ketoacidosis is essential unless
patient is in extremis: usually, there are electrolytes and acid-
Risk of a fatal reinfarction during a general anaesthetic is greatly
increased up to 6 months after MI Delay Elective procedures until then.
Concurrent drug therapy Chronic respiratory infection
Arrhythmias Coryzal symptoms
Heart failure Obesity
Hypertension Liver disease
Valvular heart disease Sickle cell anaemia
ROUTES: INH, IV, IM, PO (Rare), PR (Rare)
HALOTHANE: Volatile anaesthetic gas, with many advantageous:
Potent at relatively low concentration
Pleasant to inhale
However, its use has declined as a result of a number of disadvantages:
Associated with severe hepatotoxicity, cardiorespiratory depression,
peripheral vasodilatation and sensitisation of the myocardium to
catecholamines ( risk of arrhythmias)
Little analgesia or muscular relaxation
Can imitate malignant hyperpyrexia
ENFLURANE: Volatile anaesthetic with a similar activity to halothane, but…
Less potent at both induction and maintenance. This extends to its SEs:
Like halothane, Cardiorespiratory depression but < risk of arrhythmias.
Usually given as an adjunct to NO-Oxygen mixtures.
May Epileptiform seizures Should be avoided in epileptics.
Used at low dose for inhalational analgesia, e.g. carried by a 50% oxygen
mixture (Entonox) or at higher concentrations with other agents for
induction and maintenance of balanced anaesthesia.
NO may be best avoided for inhalational anaesthesia in following cases:
When need for high inspired oxygen concentrations
First four weeks of pregnancy
Long operations on patients with closed gaseous compartments
- there is a diffusibility volume e.g. a pneumothorax
may enlarge to compromise respiration
Cerebral vasodilation, increase in intracranial pressure
Where alternative would suffice with < atmospheric pollution
Chronic exposure to NO may interfere with folate metabolism, so --> in all
of signs of deficiency, e.g. megaloblastic anaemia, neuropathy.
ORAL AND RECTAL
CENTRAL VENOUS ACCESS
ROUTES FOR CENTRAL VENOUS CANNULATION
Central venous cannulation is performed for vascular access, total
parenteral nutrition, infusion of irritant drugs, measurement of central
venous pressure, cardiac catheterisation, pulmonary artery
catheterisation and transvenous cardiac pacing.
ROUTES FOR CENTRAL VENOUS CANNULATION INCLUDE:
Internal jugular vein
External jugular vein
WILL WESTON Page 7 of 7