Emergency Notes Flashcards
What is the acronym to assess breathing?
RATES - Rate, auscultate, trachea, effort, SpO2.
What Investigations do you order for trauma patient?
FBC, UEC< LFT< Lipase, Coags, G+H
CXR - haemothorax
FAST - Focused Assessment with sonography in Trauma - intra-abdominal blood and cardiac tamponade
Pelvic XR - Pelvic CTA
What is the coagulopathy of trauma?
A lethal triad of:
Acidosis - causes clotting factor dysfunction. Inadequate tissue perfusion in hypovolaemic shock - metabolic acidoses. Resp issues - resp acidosis
Hypothermia - platelet dysfunction, enzymatic function disrupted. Acidosis and hypothermia are synergist and when both present worsen coagulopathy more.
Haemodilution - fluid administration. Iatrogenic coagulopathy. Alterations in the coag system induced by large volumes of IV fluids or unbalanced components of blood administration.
How many stages of haemorrhagic shock are there?
4
What 8 factors change through the stages of haemorrhagic shock?
Blood loss (mL)
%Blood loss
Pulse
BP
Pulse pressure
RR
Urine output
CNS
Describe the first stage of haemorrhagic shock.
Less than 750mL blood loss (less than 15%). Pulse less than 100, BP is normal, Pulse pressure is normal or elevated, RR is 14-20, Urine output is over 30 mL/hr, CNS is slightly anxious.
Describe the second stage of haemorrhagic Shock
Blood loss 750-1500 mL, 15-30%. Pulse 100-120, N BP, decreased pulse pressure, RR 20-30, Urine output 20-30 mL/hr, Mildly anxious.
Describe the third stage of Haemorrhagic shock.
1500-2000 mL blood loss (30-40%), 120-140 PR, lowered blood pressure, lowered pulse pressure, 30-40 RR, 5-15 ml/hr of urine output, and confused.
Describe the fourth stage of haemorrhagic shock.
Over 2L blood loss, over 40%. Over 140 HR, with lowered BP and pulse pressure. Over 35 RR, Neglible urine output and confused and lethargic CNS.
What is a major trauma?
Major injury affecting more than one body system or
Injury severity score over 15.
What is the trauma call criteria?
Mechanism: Fall over 6m, high risk MVC, MBC, vehicle vs pedestrian.
Specific injuries: Flail chest, paralysis, proximal penetrating injuries or amputations, pelvic fractures, multiple long bone fractures, crushed or mangled extremity.
Physiological derangement: GCS less than 14, SBP less than 90, RR over 30 or less than 10.
Patient factors: Extremities of age, pregnant.
How to fill out the injury severity score?
Score the worst injury at each region of the body - from No injury - minor - moderate - serious - critical - unsurvivable
Total out of 75 - Head and neck, face, chest, abdo, pelvis, extremity.
What are the trauma bloods?
FBC, UEC, VBG, Group and crossmatch, Coags, Lipase, LFTs
Besides trauma bloods, what other investigations would you consider for major trauma?
ABGs, BSL, Temp, ECG, FAST US, XR, CT, diagnostic peritoneal aspirate or diagnostic laparotomy.
What does TBI stand for?
Traumatic Brain Injury
How do we classify TBI?
Primary - injury to the brain that occurs at the time of impact or insult with immediate effects, eg direct trauma to the brain, haemorrhage, contusion, axonal shearing.
Secondary - occurs as a result of insult the the brain after the initial injury, can cause worsening damage. Eg hypotension, hypoxia, anaemia, hypercapnia, electrolyte distrubance.
Or by location:
Extradural, Subdural, subarachnoid, intraparenchymal.
What clinical features can you get from TBI?
Eyes - VI nerve palsy. Ipsilateral fixed and dilated pupils, papilledema.
Cushing’s triad
Motor and sensory abnormalities
Blood or CSF from ears
Posturing
What is Cushing’s Triad and what does it indicate?
Systolic hypertension - widening pulse pressure
Bradycardia
Respiration abnormalities - decreased or irregular
Indicates transtentorial herniation.
Outline the treatment for TBI
Head CT
ABCDE + ATLS
Secure airway, intubate, C-spine precausions
Optimise ventilation, O2, EtCO2 monitoring 30-35
IVC, maintain BP, reverse anticoagulation
BSL
Look for other injuries, normothermic
Other:
Antiemetic prophylaxis - ondansetron
Seizure Prophylaxis
Sedation if combative
Increased ICP: Head elevation to 90 degrees, Mannitol, Hypertonic saline.
What is Serotonin Syndrome?
A drug related complication resulting form increased brain stem serotonin activity, usually precipitated by the use of one or more serotonergic drugs.
What drugs are associated with serotonin syndrome?
SSRI, SNRI, MAOI, TCA
Metoclopramide, Ondansetron
Amphetamines, Opioids
St John’s Wart
CNS stimulants
What symptoms are associated with serotonin syndrome?
CNS: Headache, agitation, hypomania, confusion, hallucination, coma
Autonomic: Pupil dilation, sweating, hyperthermia, tachycardia, nausea
Somatic: Akathisia, tremor, clonus, myoclonus, hyperreflexia
Severe: Seizures, metabolic acidosis, rhabdomyolysis, Renal failure, DIC, Malignant hyperthermia.
What criteria are used for serotonin syndrome?
The Hunter Serotonin Toxicity Criteria
What is the antidote used in serotonin syndrome?
Xyproheptidine, Olanzipine, Chlorpromazine. Used for mild-moderate refractory to benzos.
How do you manage serotonin syndrome?
Cessation of serotoninergic medications
Supportive management - Benzodiazepines for clonus
Atypical antipsychotics with serotonin antagonist activity
Cyproheptadine is an antihistamine with serotonin antagonism in severe cases
Hyperthermia - benzodiazepines for muscle hyperactivity and vecuronium if severe.
Prognosis of serotonin syndrome?
Most symptoms resolve within 24 hours. But deaths have occurred.
What is Neuroleptic Malignant Syndrome?
A life threatening reaction that occurs due to Neuroleptic or antipsychotic medications.
What drugs can cause NMS?
- Haloperidol, droperidol, promethazine, chlorpromazine.
- Clozapin, olanzapine, risperidone, quetiapine
- Dopaminergic drugs: Levodopa on cessation, metoclopramide.
What is the pathophysiology of NMS?
Blockade of dopamine receptor D2 leading to abnormal function of the basal ganglia and muscular Sx. Atypical antipsychotics also affect serotonin, GABA and glutamate worsening the syndrome.
What are the symptoms of NMS?
FEVER - fever, encephalopathy, Vital instability (autonomic Sx), Elevated Enzymes (CK, rhabdomyolysis), Rigidity of muscles.
Can be agitated, delirious, coma, hyperkalaemia, renal failurek, seizures.
Onset within 1 week, Reaches peek in approx 3/7. Can last 8hrs - 1 month.
How to treat NMS?
Cessation of causative medication
If hyperthermic - active cooling
Symptomatic management
Dantroline for severe rigidity
?Bromocyptine
What is anticholinergic syndrome?
The inhibition of cholinergic neurotransmitters at muscarinic receptor sites following ingestion of certain medications.
What are the causative agents of anticholinergic syndrome?
Anti-histamines, anti-Parkinson’s, Atropine, Anti-spasmodics, Skeletal muscle relaxants.
What are the symptoms of anticholinergic syndrome?
Flushing, dry skin
Mydriasis
Altered Mental Status
Fever
Tachycardia and HTN
Myoclonic jerking
Urinary retention
Dysrhythmias
Seizure
“Mad as a hatter, Dry as a bone, Red as a beet, Hot as a desert, Blind as a bat”
What is the treatment for anticholinergic syndrome?
Cessation of causative agent
Supportive management
Physostigmine: Reversible acetylcholinesterase inhibitor
Investigations for anticholinergic toxicity?
ECG
Temp
UEC
CK
Bladder scan
Toxicology
What is the treatment for anticholinergic toxicity?
IV fluids
Activated charcoal
Whole bowel irrigation if severe
Diazepam for agitation
Avoid anticholinergic drugs
Physostigmine - reversible acetylcholinesterase inhibitor, half life 4 hours. Pts get better then deteriorate. Symptomatic management.
What are extra-pyrimidal symptoms?
Drug induced movement disorders/symptoms that occur as a result of certain medications.
What drugs cause EPS?
Typical and atypical antipsychotics, Metoclopramide, Antidepressants
What symptoms are included in EPS?
ADAPT: Acute Dystonia, Akathisea, Parkinsonism, Tardive Dyskinesia
What is acute dystonia?
Sustained or repetitive muscle contractions reslting in twisting and repetitive movements or abnormal fixed postures
What is akathisia?
Feeling of inner restlessness and need to be in constant motion
What is parkinsonism?
TRAP - Tremor, rigidity, akinesia (bradykinesia), postural instability.
What is tardive dyskinesia?
Involuntary repetitive body movements.
How do you monitor for EPS?
Abnormal Involuntary movement scale
Tool for monitoring antipsychotic effects
What is the treatment for EPS?
Dose titration or cessation of causative medicine.
Anticholinergic medications
Akathisia may require B-blockers or benzos.
What symptoms can you get if you stop antidepressants too quickly?
FINISH
Flu like illness
Insomnia
Nausea
Imbalance
Sensory disturbance
Hyperarousal
What is acute cholecystitis?
Inflammation of the gall bladder
What are the causes of acute cholecystitis?
Calculous 90% of the time.
Acalculous can be from trauma, sepsis, blood transfusion, narcotics, ABs
What are the symptoms of acute cholecystitis?
Epigastric pain –> RUQ pain, worse on movement.
Billiary colic
Pain preceded by fatty foods or EtOH
Fevers, Rigors, Chills
N+V
Anorexia
Jaundice 10%
Shock
Charcot’s Triad and pentad
What are Charcot’s Triad and pentad?
Tirad: RUQ Pain, Fever, leucocytosis
Pentad: Triad + Hypotension, altered consciousness.
What clinical features to look for acute cholecystitis?
RQU pain worse on palpation
Garding
Murphey’s Sign
Palpable gall bladder
Febrile
Tachycardia
Peritonism
What investigations to do for acute cholecystitis?
FBC
CRP
LFTs (cholestatic picure)
Increased conjugated bilirubin
US - Gall bladder wall thickening or oedema (double wall sign)
HIDA scan
CT when US unreliable (obesity)
MRI when pregnant
Cholangiogram: MRCP + ERCP + PTC (Magnetic Resonance Cholangiopancreatography + Endoscopic Retrograde cholangiopancreatography + Percutaneous transhepatic Cholangiography
Treatment for Acute cholecystitis?
Supportive management: IV fluids, analgesia (buscapan), antiemetics
IVABs
Laparoscopic or open cholecystectomy. If pain settles, DC and elective. If persisten - admission and inpatient..
What are the causes of acute pancreatitis?
IGETSMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Malignancy and mumps
Autoimmune
Sting - bee, scorpion, spider
Hyperlipidaemia, hypertriglyceridemia, hypercalcaemia, hyperthyroidism
ERCP
Drugs (thiazides, frusemide, azathioprine, oestrogen).
What are the symptoms of acute pancreatisi?
Epigastric pain, dull and stead, progressive.
LUQ or RUQ pain
Radiation to back
N+V
Fever, chills
Shock
What clinical features are you looking for acute pancreatitis?
Abdominal tenderness
Guarding
Abdominal distension
Reduced bowel sounds
Peritonitis
Hypotension and SIRS Sx
Grey-Turner’s Sign - haemorrhagic discolouration of Flanks - retroperitoneal
Cullen’s Sign - haemorrhagic discolouration of umbilicus
Hypocalcaemia
What criteria do you use for acute pancreatitis?
Atlanta Criteria: 2/3
Classic abdominal pain
Lipase 3x upper limit normal
Imaging suggestive of pancreatitis
Investigations for acute pancreatitis:
Bloods: FBC, CRP, Lipase, LFTs, Electrolytes, UECs, urine output.
Imagine: US, CT, MRI, ?CXR to exclude other pathology.
How to treat acute pancreatitis?
Fluid Resus
Analgesia, NPO, Antiemetics
Electrolyte monitoring and replacement
ABs (Tazocin)
Surgical intervention when severe or due to gallstones
What are the complications of acute pancreatitis?
Peripancreatic fluid collection, pseudocyst, pancreatic abscess
Intra-abdominal infection
Infected necrosis
Splanchnic thrombosis
Abdominal compartment syndrome
Pleural effusion
Shock
What is appendicitis?
Inflammation of the veriform appendix usually due to appendiceal luminal obstruction.
What symptoms can you get for appendicitis?
Epigastric pain, severe, intermittent, dull. Moves to the RLQ, sharp pain, increasing in severity, constant.
N, V, A
Fever, malaise
Constipation is late.
What clinical features do you look for in appendicitis?
Peritonism, guarding, rigidity, rebound tenderness, diminished bowel sounds on the right, shock.
McBurney’s Point - Pain on palpation - worse 3.8-5cm along line ASIS to umbilicus
Rovsing’s Sign - RLQ pain with palpation of LLQ
Psoas Sign: Pt lies on left and passive attempt to extend R hip, painful is positive
Obturator sign: Internal rotation of thigh causes pain
Markle sign: Pain in abdominal cavity when dropping from toes to heels.
What score do we use for appendicitis?
MANTRELS score:
Migration of pain to RLQ
Anorexia
N+V
Tenderness in RLQ (2)
Rebound tenderness
Elevated Temp
Leucocytosis (2)
Shift of WBC to left
What investigations to do for appendicitis?
FBC
Inflammatory markers
UA
Pregnancy test
US
CT
Diagnostic laparoscopy
Treatment for appendicitis?
Analgesia
Fluid resus
NPO
IVABs (gm-ve and anaerobic coverage)
Lap appendectomy
What are the types of acute infectious diarrhoea?
Actue: 3 days to 14 days
Chronic: Over 14 days loose stools
What are the symptoms of gastroenteritis?
Diarrhoea, N+V, Fever, Generally unwell, crampy abdominal pain, dehydration
What are the causes of gastroenteritis?
Viral: Norovirus, Rotavirus, Adenovirus
Parasitic: Giardia lamblia, entamoeba histolitica
Bacterial: E Coli, Campylobacter Jejuni, Salmonella, Shigella, Clostridium Difficile
What is the treatment for gastroenteritis?
Fluid and electrolyte replacement
Bacterial: ABs.
Causes of small bowel obstruction?
HAVIT: Hernia, Adhesions, Volvulus, Intussusception, Tumour
What is a TIA?
Sudden onset focal neurological Sx caused by transient decreased blod flow, lasting for less than 24 hours resolving with no permanent neurological symptoms.
Describe the pathophysiology of a TIA.
TIAs are characterised by a temporary reduction or cessation of cerebral blood flow in a psecific neurovascular distribution as a result of partial or total occlusion - typically from an acute thromboembolic event or stenosis of a small penetrating vessel that resolves spontaneously with no remaining neurological deficit.
What are the causes of TIA?
Atherosclerosis
Embolic source - AF, valvular disease, mural thrombus, paradoxial embolism
Arterial dissection
Hypercoagulable states
Unknown
What are some risk factors for TIAs?
AF
hypercoagulability
valvular disease
carotid stenosis
CCF
HTN
DM
EtOH
Smoking
Age
What score can be used for TIA?
ABCD2 score - risk stratification for CVA post TIA. 6-7 = 8% risk of CVA within 2 days.
Age over 60
BP over 140/90
Clinical features:
Unilateral weakness (2)
Speech impairment without unilateral weakness
Duration
over 60mins, (2)
10-59 mins (1)
Diabetes
What investigations for TIA?
FBC, UEC, Coags, Head CT - non-con, CT angiogram, MRI, ECG - cardioembolic cause
How to treat for TIA?
Treat as a stroke until proven otherwise.
Antiplatelet - aspirin 100 mg or clopidogrel 75 mg
Anticoagulant: NOACs
Mx of risk factors / causes
What is an ischaemic stroke?
Sudden loss of blood circulating in an area of arterial blockage causing ischaemia, cell death and corresponding loss of neurological function. Acute neurological deficit lasts over 24 hours.
What are the causes of ischaemic stroke?
Thrombus
Embolic - clot, cholesterol, fat, air, placenta, septic, malignant
Cardioembolic
Vasculitis
Hypercoagulability
Dissection
Moyamoya disease
What are the DDx for stroke?
TIA, hypoglycaemia, seizure, Bell’s palsy, infection, brain neoplasm, migraine
What is an extradural haemorrhage?
Bleeding between the inner surface of the skull and outer dura mata.
What is an extradural haemorrhage associated with?
Commonly with trauma.
Frequently associated with a skull # of the temporal bone 75%
Tearing to the middle meningeal artery 75%
Can occur due to torn venous sinus and overlying #
What symptoms are common with extradural haemorrhage?
Hx of head trauma
LOC
Lucid interval
Headache
N+V
Seizure
Decreased level of consciousness
What clinical features are common with extradural haemorrhage?
skull contusion, laceration, bleeding
Decreased level of Consciousness
Cushing’s triad
Hemiplegia
Postruing
Sluggish pupils
CNIII palsy - oculomotor. Dilated ipsilateral pupil, can progress to bilateral.
CNVI Palsy - long course. Failure of lateral gaze
Fixed dilated pupil - ipsilateral or bilateral
What investigations to do for Extradural haemorrhage?
Trauma bloods
Non-con Head CT
