Acute Medicine Flashcards
3,4–Methylenedioxymethamphetamine (Ecstasy) MDMA
-This causes anxiety, restlessness, hyperthermia, ataxia, blurred vision, confusion and syncope.
- It can cause palpitations and chest pain.
- Tachycardia, hypertension
- GI symptoms include dry mouth, nausea, abdo pain.
- It also causes pupillary dilatation
Diamorphine (Heroin)
- Mild hypotension and mild bradycardia are commonly observed with heroin use.
- ->These are attributable to peripheral vasodilation, reduced peripheral resistance and histamine release, and inhibition of baroreceptor reflexes.
- Respiratory depression, due to heroin’s effect on the brain’s respiratory centres is a hallmark.
- -> However, the presence of tachypnoea should prompt the search for complications of heroin use such as pneumonia, pulmonary oedema, pneumothorax; or an alternative diagnosis such as shock, acidosis or CNS injury.
Gamma Hydroxybutyrate (Grievous Bodily Harm, GHB).
- It has a myriad of neurological effects.
- After GHB ingestion, the patient may have a period of euphoria that is rapidly followed by a period of profoundly depressed level of consciousness (hence its reputation as a date rape drug).
- This may progress to coma with a Glasgow Coma Scale of 3.
- GHB intoxication characteristically produces episodes of agitated delirium that can precede or follow the period of stupor or coma.
- Seizure like movements and myoclonus are common. - More commonly would cause bradycardia and hypotension.
Ketamine (special K)
- Ketamine is a rapid acting general anaesthetic producing an anaesthetic state
- Characterised by profound analgesia, normal pharyngeal/ laryngeal reflexes, normal or slightly enhanced skeletal muscle tone, cardiovascular and respiratory stimulation, and occasionally a transient and minimal respiratory depression.
- It does cause pupillary dilatation
Neuroleptic malignant syndrome
See syndromes
Serotonin syndrome
See syndromes
Naloxone
Used for opiate OD
Sodium bicarbonate
Used in TCA overdose
- Plasma alkalinization and TCA plasma protein binding
- Intracellular alkalosis and TCA receptor binding
- Intracellular hypopolarization
- Sodium load
- Correction of metabolic acidosis
- Volume loading
- Other pharmacokinetic effects
Digoxin OD
- Digoxin inhibits sodium ATPase
- Bradycardia
- Hyperkalemia (early)
- Confusion
- Arrythymia
ECG changes show evidence of AV dissociation with 1st-3rd degree heart block
TCA overdose
Rapid onset 1-2 hours
- tachycardia
- Hypotensiom
- Sedation and comas
- Seizures
- -> if QRS >100ms
QT prolongation –> broad complex dysarrythmia
–> if QRS >160ms predictive of VT
- cardiotoxic effects by:
1. block myocardial Na+ fast channels - -> QRS prolongation, tall R wave in aVR
2. inhibit K+ channels - -> QTc prolongation
- -> direct myocardial depression
3. blockade of muscarinic (M1), histamine (H1) and alpha adrenergic receptors
Rx:
IV sodium bicarbonate (Plasma alkalinization and TCA plasma protein binding, Intracellular alkalosis and TCA receptor binding, correction of metabolic acidosis among other things)
Beta blocker/calcium channel blocker overdose
CLINICAL FEATURES:
proportional to the type and amount ingested
CVS: hypotension, bradycardia, AV block, heart failure
RESP: bronchospasm
METABOLIC: hypoglycaemia, hyperkalaemia
NEURO: stupor, coma, seizures
MANAGEMENT
ECG can show:
- sinus bradycardia
- abnormal AV node conduction
- an accelerated junctional rhythm
Rx (antidote):
-Glucagon as first line followed by high dose insulin euglycemic therapy and dextrose –> glucose used as fuel in the heart to increase ionotropy (which CCB OD decreases)
Resuscitation:
- fluid
- beta-agonists
- vasopressors
- atropine
- pacing
Acid-base and Electrolytes Balance:
- hypoglycaemia -> dextrose
- hyperkalaemia: Ca2+ gluconate, dextrose-insulin, -NaHCO3, dialysis, salbutamol
Decontamination:
-activated charcoal if <1 hour and no C
Two beta-blockers require special consideration:
— propanolol -> causes sodium channel blockade -> QRS widening -> treat with NaHCO3
— sotalol -> causes potassium efflux blockade -> long QT -> monitor for Torsades
Hypertensive crisis
RX: Nitroprusside
Colchicine overdose
- Plant based alkaloid
- Rapidly absorbed
- peak serum concentration after 30mins- 3 hours
- 50% protein bound (haemodialysis and haemodilution is not helpful)
- Gastro symptoms within 24 hours (abdo pain, N+V, diarrhoea
- Later features 1-7 days are tachypnoea, low calcium, low po4, hypovolaemia, haematological effects (e.g. leukopaenia, thrombocytopaenia), cardiac dysrhythmias,renal failure and liver damage.
-The cause of death is usually
progressive multiple organ failure and sepsis.
Rx:
- activated charcoal to try and absorb ASAP as no antidote
- High mortality
- -> >0.5mg/kg dose assoc with 10% mortality
- -> >0.8mg/kg dose assoc with 100% mortality
- -> 7mg/kg dose with kill an adult
When activated charcoal not useful or CI
P- Pesticides, petroleum distillates H- Hydrocarbons, heavy metals, > 1 hour post ingestion A- Acids, alkali, alcohols I - Iron L - Lithium S - Solvents
In resus of unknown ingestions
Three S’s
S-seizures –> midazolam. DO NOT give phenytoin as can worsen some ingestions
S-sugar –> treat hypoglycemia
S- shivering –> treat hypothermia
Decontamination
Induced emesis and Gastric lavage is not usually done in kids
Activated charcoal and whole bowel irrigation is very rarely done in kids
-consider if risk assessment predicts severe or life threatening toxicity where supportive care or an antidote is alone not enough to ensure a good outcome
List of meds where “two pills can kill” so needs overnight continuous monitoring
- Sodium channel blockers:
- choloroquine and hydroxycloroquine
- PROPANOLOL
- TCA’s
- atropine
- Calcium channel blockers:
- VERAPAMIL
- DILTIAZEM
- Theophylline SR
- Sulfonylureas (glipizide, glicazide)
- Amphetamine and ecstasy
- Opiates:
- Methadone
- Morphine
- Oxycodone
Drugs where a “mouthful can kill”
- Organophosphates/carbamates
- insecticides
- Hydrocarbons
- kerosene
- eucalyptus oil
- solvents
- Camphor and its oil
- Paraquat = pesticide
- Napthalene
- moth balls (only one needed to kill)
Drugs where fetal risk > maternal risk
- Carbon Monoxide
- Methaemaglobin inducing agents
- napthalene
- dapsone (topical and oral antibiotic used to treat leprosy)
- lead
- salicylates
Anticholinergics
- Tachycardia, HTN
- normal respiration
- hyperthermia
- DILATED pupils
- quiet bowel sounds and urinary retention
- dry and red skin
- CNS altered, agitated/ hypervigilant
e.g
Atropine, scopalamine, benztropine
TCAs
some antihistamines –> chlorpromazine among others
Cholinergics
- No change in HR/BP, Respiration or temperature
- PINPOINT pupils
- Hyperactive bowel sounds
- Confusion/coma
SLUDGE ( hyperSalivation, Lacrimation, Urination, Diarrhoea, GI upset, Emesis)
e. g
- organophosphates
- mushrooms
- pesticides
- physostigmine
Opioids
- bradycardia, hypotension
- respiratory depression
- hypothermic
- PINPOINT pupils
- quiet bowel sounds and urinary retention
- Dry skin
- Drowsy/fluctuating GCS
e. g
- morphine
- codeine
- tramadol
- fentanyl
- methadone
- oxycodone
Sympathomimetics
- Tachycardia and HTN
- Tachypnoea
- Hyperthermia
- DILATED pupils
- Wet skin
- CNS altered/agitated
e. g
- Caffeine
- Cocaine
- amphetamines
- methamphetamines
- Ritalin
- MDMA
Sedative/hypnotic
- bradycardia and hypotension
- Respiratory depression
- Hypothermia
- NORMAL pupils
- Quiet bowel sounds
- Dry skin
e. g
- anti-anxiety medications
- muscle relaxants
- benzodiazepines
- barbituates
- other anti-seizure medications
Hallucinogens
- Tachycardia, HTN
- Normal Respiration
- Hyperthermia
- DILATED pupils (mydriasis)
- Hallucination, synesthsia, agitation, nystagmus
Antidote for Isoniazid
Pyridoxime
Antidote for Methemoglobinemia
Methylene blue
Antidote for CCBs
Calcium gluconate/chloride
Glucagon
Insulin/glucose
Antidote for Ethylene glycol (antifreeze)
Ethanol, Fomipazole
Antidote for Iron
Desferroximine
Antidote for Sulphonylureas (causes oral hypoglycemia)
Octreotide - inhibits insulin release
Antidote for Benzodiazepines
Flumazenil - blocks benzodiazepine receptor site
Antidote for Beta blockers
Glucagon
Calcium gluconate
Insulin/glucose
Treatment for cholinergics (classically organophosphates)
IV atropine (which is an anticholinergic)
Management of unidentified ingestion
- Admit for 12 hours minimum observation
- Check BSL at:
- presentation
- if sx
- at dc - IVL if toxicity
- Clear documentation of signs of toxicity
- monitor LOC, vital signs, BSL
- Cardiac monitoring I above abnormal
- Discharge in daylight only
Take home point: If takes only ONE PILL
- child will not come to harm even if high dose UNLESS
- Colchicine
- Sulphonylurea
Take home point: If >4 hours post ingestion
- if nothing bad has happened, nothing bad is likely to happen EXCEPT:
- Paracetamol TABLETS
- SLOW release formations
- Methanol
- Ethylene glycol (Antifreeze)
Abdominal trauma
- MOST kids with major abdominal trauma DO NOT require surgery –> Only 15% require surgery
- Of children admitted to trauma centres only 8% have documented abdominal injuries
- Abdominal trauma is NOT a major cause of traumatic death in childhood (normally Head and thoracic injuries)
- BUT abdominal trauma is the most UNRECOGNIZED cause of fatal injuries
- Abdominal injury occurs in approx. 22% of children with FATAL injuries
Haematuria in trauma
- Can result from anywhere along the GI tract
- In absence of genital injury, EXTERNAL urethra injuries are unlikely
- If >30 rcc requires abdominal CT scan to look for genitourinary injury
- USS can MISS renal injury –> CT is gold standard
Head trauma - Extra dural haematoma
- an acute bleed between the dura mater and the inner surface of the skull
- most commonly caused by skull trauma in the temporoparietal area
- associated with skull fracture
- “lemon” shaped-bleed, seen on CT and MRI imaging
- Do not cross suture lines
- If the extradural haematoma continues to increase in size = raised ICP –> midline shift –> tentorial herniation
- -> brainstem death
Signs and symptoms:
- Early signs
- Severe headache onset or an hour or so later
- Initial loss or fluctuance in consciousness
- ->May present vaguely as tiredness or confusion or combativeness
- PERIOD OF LUCIDITY after initial loss of consciousness
- ->Usually lasts between 6 and 8 hours but can last up to days
- Late signs
- Rapid deterioration and loss of consciousness (raised ICP and herniation
- Cranial nerves palsies
- ->CNIII (oculomotor nerve) palsy may result in fixed dilation of the ipsilateral pupil.
- Muscle weakness
- -> Hemiparesis typically begins on the contralateral side
- ->Hemiparesis may become bilateral as the ICP increases and the brainstem becomes compressed.
- ->Ipsilateral hemiparesis can also occur through Kernohan’s phenomenon (extensive midline shift of the brain due to mass effect from the growing extradural haematoma)
- Upper motor neuron signs
- Positive Babinski’s sign, hyperreflexia and hypertonia
- Cushing’s triad
- This is characterised by bradycardia, hypertension and deep/irregular breathing
Resulting ultimately in respiratory depression and death
Head trauma- Subdural haematoma
- Blood in potential space between the dura and arachnoid mater
- stretching and tearing of bridging cortical veins as they cross the subdural space to drain into an adjacent dural sinus
- SDH can happen in any age group –> infants in NAI, young adults in MVA
- 75-85% occur bilaterally in infants
- Isolated interhemispheric/parafalcine subdural haematomas are seen more frequently in children and are common in cases of NAI.
- Commonly co-exist with intracerebral contusions
- Occasionally happen in coag disorders (AVM, anticoagulation therapy, bleeding disorder)
- Typically crescent-shaped
- usually more extensive than extradural haematomas. - CROSS sutures
- Dx made by CT
Head trauma - intraparenchymal bleed
- aka intracerebral haemorrhage
- Locations include: ◦basal ganglia ◦thalamic ◦pontine ◦cerebellar ◦lobar
- There are different causes, not just trauma:
◦hemorrhagic venous infarct
◦hypertensive hemorrhage
◦hemorrhagic transformation of an ischemic infarct - Can see on CT, MRI
- CTA can be done if suspect vascular malformation
Nasal trauma
- Often presents with injury to the face, marked swelling, deformity and epistaxis
- XR of nasal bones are NOT helpful in acute management of nasal #
- True # can be hard to assess clinically initially due to marked swelling –> often nose will look deformed without a #
- -> need to wait 4-5 days for swelling to subside
- -> Then need to see GP at 5 days and ENT urgently within 7 days if noted once swelling has subsided
- Septal haematoma
- -> if not identified and treated quickly can get cartilage NECROSIS and septal perforation
- -> worst outcome is saddle nose
- -> identify by looking in nose with otoscope or nasal speculum
Neurogenic shock
- Neurogenic shock is due to loss of sympathetic vascular tone and happens only after a significant proportion of the sympathetic nervous system has been damaged
- Occurs within 30 mins of injury
- Resolution takes up to 6 weeks
Excessive parasympathetic activity:
- bradycardia
- peripheral vasodilatation and decreases vascular tone resulting in reduced systemic vascular resistance
- -> Hypotension
- poor perfusion of tissues and impaired cellular metabolism BUT skin is STILL WARM (vasodilatation)
- Unable to regulate temperature
Causes:
- Spinal cord injury ABOVE T5
- Spinal anaesthesia
- Vasomotor center depression such as severe pain, drugs or hypoglycaemia
Mx:
- Airway support
- IVF
- Atropine for bradycardia
- vasopressors for BP
SCIWOR
-spinal cord injury w/o radiological findings
SCIWOR
- Spinal cord injury w/o radiological findings
- Occurs far more often in children (hypermobility of the spine) esp in <8 year olds
- If injury with transient neuro findings –> SCIWOR can occur later ( 1/4 present delayed up to 4 days)
- Sx of SCI without XR or CT scan findings
- Associated with flexion/extension injuries –>sports injury, MVA, NAI
- May present with neurogenic shock
- Injury can be incomplete (some sensation and motor preserved or complete)
- Dx made by MRI
High risk:
If transient neurological signs which have resolved with a normal neuro exam in a child <8 years old or high risk mechanism (MVA, fall from height)
Mx:
- Immobilisation of the spine to prevent further injury
- Cervical spine immobilisation (moving cervical spine moves the rest of spine)
- ABC’s supportive care
- Treatment with Methylprednisolone is controversial
Eye injuries - superior wall orbit #
- Trauma i.e cricket bat or ball
- blow out # of superior ridge of orbit
- Often results in a “pulsating proptosis” due to communication between the orbit and the intracranial cavity
- Nerve entrapment resulting in decreased ocular movement –> patient cannot look AWAY from the fracture
- At times haemorrhage can:
- displace eye AWAY from #
- restrict ability of eye to look TOWARDS #
Dental injuries - Complete Avulsion
- totally out of socket
- IF primary tooth (baby) DO NOT replace as can cause damage to developing bud of permanent tooth underneath
- If not sure if primary or permanent tooth treat as if permanent tooth below
- Permanent tooth
- prognosis for survival inversely proportional to time of tooth out of socket (85-97% at 5min and near 0% at one hour)
- Put tooth back in socket ASAP (ideally within 15 minutes –> can be longer if tooth placed in cold milk
- First irrigate any clot in the socket gently
- Rinse tooth in cold milk/saline/tap water then replace in clean socket gently –> have child either hold in place, or bite down gently with gauze or tea towel
–> refer to paediatric dentist for mx (splinting, abx, root canal)
factor VIII deficiency(A) and head injury
factor IX deficiency (B) and head injury
-All significant head injuries must be considered nontrivial unless proven otherwise by observation and CT/MRI –> still low threshold for Rx even with normal MRI
- If in doubt treat with factor VIII/ IX
- Treatment takes precedence over imaging
- ALWAYS give factor VIII/IX to correct to 100% REGARDLESS of evidence of bruising or swelling
- -> bolus then infusion
- Rx at least 3 days
- If ICH needs Rx up to 3 weeks then prophylaxis
- Can get DELAYED bleed following HI up to 3-4 weeks so be aware of signs
Factor VIII deficiency and severe/life threatening bleeding
Factor IX deficiency (B) and head injury
●Bleeding in the central nervous system
●Ocular bleeding
●Bleeding in the hip
●Deep muscle bleeding with neurovascular compromise or the potential for neurovascular complications
●Intra-abdominal bleeding
●Bleeding that could affect the airway (eg, into the throat or neck)
●Bleeding severe enough to result in anemia and potentially require red blood cell transfusion(s)
●Prolonged bleeding that is not adequately responding to home-based therapy
●Iliopsoas bleeding
●Significant injuries such as motor vehicle accidents or falls from distances of several feet or more
Patients MUST keep levels above 50% or more therefore MUST initially correct to 100% with factor VIII
Infected wounds - organisms
- Pasteurella multicoda
- animal bites (esp cats/dogs)
- Eikenella corrodens
- slow growing (hard to grow in lab)
- about 30% infections post human bite
- Gram negative rod
- human bites, head and neck infections
- Infection from about 1/52 post injury
- Can cause serious infection including chronic abscesses
- Often mixed with strep
- Rx with penicillins and 3rd gen cephs
- Resistant to cephalexin
- streptobacillus moniliformis
- Rat bites
- Staph Aureus
- about 30% post human bite
- more rapid onset than Eikenella –> presents usually <1 week
High risk of intracranial injury
- focal neurological signs
- > 5 episodes of vomiting or lasting >6 hours
- seizure
- signs of depressed or basilar skull #
- penetrating skull injury
- irritability
- bulging fontanelle
- Loss of consciousness 1 minute or more
Post-traumatic seizures
- immediate, early or late
- Immediate seizures:
- from direct application of energy to cortex as a result from traumatic impact
- Occur within sec
- Indicate high force blow
- Not necessarily assoc with focal intracranial injury
- Early post-traumatic:
- occur minutes to hours post injury
- are a frequent manifestation of irritable focus in the brain
- often assoc with cerebral contusion or ICH
Chest injury and young children
- In < 2 years = more bendy ribs
- -> In heavy force impact injury (i.e car) most likely to get PULMONARY CONTUSIONS rather than pneumothorax/haemothorax or rib #
Drowning poor prognostic factors
●Duration of submersion >5 minutes (most critical factor)
●Time to effective basic life support >10 minutes
●Resuscitation duration >25 minutes
●Age >14 years
●Glasgow coma scale <5 (ie, comatose)
●Persistent apnea and requirement of cardiopulmonary resuscitation in the emergency department
●Arterial blood pH <7.1 upon presentation
Drowning
- Common cause of accidental death
- Higher in low and middle income famililies
Risk factors:
●Inadequate adult supervision
●Inability to swim or overestimation of swimming capabilities.
● Hypothermia (but decreases risk of cerebral hypoxia)
●Risk-taking behaviour
●Use of alcohol and illicit drugs
●Concomitant trauma, stroke, or myocardial infarction.
●Seizure disorder or developmental/behavioral disorders in children
● Prolonged QT
- Cerebral oedema from hypoxia is usually cause of death
- For hypothermia to be protective to the brain it MUST precede the onset of hypoxic injury
- Survival rates from cardiac arrest are 20-30%
- There is NO clinical difference between salt and fresh water drowning
- The KEY predictor of outcome is mental status after drowning
Eschar separation
- is a slough or piece of dead tissue that is cast off from the surface of the skin, particularly after a BURN injury (i.e electrical burn)
- Occurs at about 2-3 weeks as new blood vessels are forming
- important as this is the time of greatest risk of haemorrhage from the labial artery
Lightening injury
*Deafness
- Cardiac
- prolonged QTc and arrhythmia occurs within hours, often non-fatal
- can get initial arrhythmia from VF or asystole causing cardiac arrest at time of lightning strike
- Skin
- burns particular to mouth if children chew on cables or wires
- Renal
- Rhabdomyolysis
- CNS
- Manifestations may include loss of consciousness, weakness or paralysis, respiratory depression, seizures, autonomic dysfunction, and memory disturbances
- Peripheral neuropathy –>Onset can be delayed for days, mixed sensory and motor and can be patchy
Patients hit by lightning may present with pupils that are fixed and dilated or asymmetric due to autonomic dysfunction. As a result, fixed, dilated, or asymmetric pupils should NOT BE A REASON to stop resuscitation
Burn injury
- Full thickness burns
- Don’t hurt
- Don’t blanch
- Have a pale centre (zone of coagulation)
*Modified rules of nine for TBSA: Head = 18% Front = 18% Back = 18% Arm + hand = 9% (18% for both arms and hands) Leg = 14% each leg
- If TBSA >10% need fluid resus
- -> 3-4mls/body weight/%burn in the first 24 hours from burn AND maintenance on top
- At risk of hyponatremia secondary to loss through burns
- For large burns electrolytes need to be monitored every 4-6 hours
- Suspect inhalational injury in ANY situation where any burn occurs in a CLOSED space i.e house fire
- -> children are at increased risk of SUBGLOTTIC injury as airways smaller + airways more easily compressed from external oedema of the neck
- -> stridor and respiratory distress are ABSOLUTE INDICATIONS to tube
- Early fatality most often due to shock
- Late fatality most often due to infection
Inhalational injury
3 types
- Supraglottic
- breathing hot gases esp in enclosed space
- oedema and desquamation of mucosa => airway obstruction
- Subglottic
- inhaled combustion products and vapourised chemicals
- Creates acid or alkali products which are toxic to mucosa
- rare due to efficient upper airway heat exchange in this area
- Systemic toxic injuries
- CO poisoning or other systemic intoxication
- look for
- -> burns around face or mouth
- ->carbonaceous sputum or cough
- -> stridor/hoarseness
- -> confusion/decreased LOC
If in doubt TUBE
First aid Rx of burns
- First aid is effective up to 3 hours following burn
- Cooling should occur for 20 minutes
- If running water is used, optimal temperature is 18 degrees
- DO NOT use ice packs or the like
- Appropriate first aid can stop progression of burn in zone of stasis (potentially salvable)
- Zone of coagulation (pale are at centre of burn) is NOT salvable ( Full cellular necrosis)
-REMEMBER to cool CREASES!
Jackson burn model
- Imagine an egg
- Outer circle
- Zone of hyperemia
- Dilated capillaries in response to inflammatory mediators
- WILL recover without intervention - Middle circle
- Zone of Stasis
- Slow circulation –> if untreated will become necrotic
- Can recover with GOOD first aid (cooling) - Inner circle
- Zone of coagulation (egg yolk)
- Full necrosis = stuffed
Half life of sedation
- IV ketamine
- 1/2 life 2-3 hours
- peaks at 1 min
- IV propofol
- 30-60 mins
- oral midaz
- 2-4 hours
- Oral chloral hydrate
- 8-10 hours
- Inhalant Seroflurane
- minutes
Ketamine in sedation
Induces bronchodilation
Good analgesia and amnesic
- side effects
- Laryngospasm is NUMBER ONE caution (transient)
- Tachycardia
- Bronchodilation
- HTN
- vomiting
- hypersalivation
- nightmares
Unique side effect of fentanyl
- other than normal side effects of opioids = chest wall rigidity
Side effects Propofol
- CVS and resp depression
- pain at injection site
- NOT an analgesic
Side effects Midaz
- anterograde amnesia
-sedation
anxiolysis
-anticonvulsant - resp depression
- paradoxical effect
Nitrous oxide
Entonox 50:50 mix o2 and N20
- Useful in small painful procedures
- CI
- Gas filled space –> pneumothorax and bowel obstruction
- Severe HI (risk of pneumocranium)
- Intoxication, decreased LOC
- Pregnancy
- Requiring > 50% oxygen
- side effects
- vomiting 5-10%
- dysphoria 1%
Pericarditis
Often viral
- can be constrictive or not
- friction rub
- inflammation
- NOT significant fluid accumulation = NOT constrictive
- NOT Constrictive (not a lot of fluid accumulation)
- ST elevation
- T wave inversion
- clear lung fields
- CONSTRICTIVE = accumulation of pericardial fluid
- Decrease in precordial voltages
- Increased in cardiac silhouette
Myocarditis
- Inflammatory disease of myocardium
- Often viral (esp cocksakie, adeno, echovirus)
- Other viruses include CMV, Hep C, HIV, influenza, parainfluenza, MMR, parvovirus and varicella
- Other causes include: drug tox, drug hypersensitivity, immune mediated such as rheumatic fever and Kawasaki
Presentation:
- unwell
- constitutional sx
- heart failure
- resp distress
- GI sx
- dysarrthymias –> AV conduction, junctional, sinus tachy
- Chest pain –> ischaemia or concurrent pericarditis
Results in:
- Decrease in myocardial function
- increased pre-load and increased end diastolic vol
- Poor contractility
- inflamed and damaged muscle
- Concomitant enlargement of the heart
- Increased atria, pulmonary vein and arterial pressures
- -> results in pulmonary oedema and heart failure
Signs of:
- Low CO
- tachycardia, weak pulse, cool peripheries, poor CRT, mottled skin
- Muffled HS (esp if pericarditis too)
- extra HS S3
- AV valve regurgitation (MV, TV)
- Hepatomegaly, oedema, raised JVP if older
- Rash
- CXR
- pulmonary oedema
- cardiomegaly
- ECG - see separate card
ECG changes of myocarditis
- Low voltages QRS
- Pseudo infarction pattern
- -> pathological q waves
- -> poor progression of R waves in precordial leads (V1-V6)
- -> T wave inversion or flattening
- -> LVH
- -> prolonged PR or QT interval
- -> PVCs, tachycardias (sinus, junctional, VT), AV block
SVT
- If poor perfusion or pulses not palapable
- proceed with pulseless resus algorithm
- If pulses palpable, adequate perfusion and ABC extra ok and monitoring on + IV access
- vagal stimulation
- Ice cloth
- Ice bath (5 sec submerge)
- Carotid sinus massage - Valsalva maneuvers
- blow against thumb/ narrow straw, syringe
- head stand/ supine position with head down for 15 secs - Adenosine
- Synchronised DC with sedation
Causes of non traumatic coma
In decreasing freqs
- Intracranial infection
- anoxic encephalopathy
- status epilepticus
- metabolic derangement
- vascular lesions
In swallowed foreign bodies
- CXR
- If not radio-opaque on XR then consider barium swallow or CT if significant object
- requires endoscopic removal if in upper or mid-oesophagus or if sx
- If no sx and XR shows a coin in lower oesophageal junction give oral fluid bolus and repeat XR in 12-24 hours (as 80% of coins at LOS will pass spontaneously within 12-24 hours)
Gastric FB
- most pass in 4-6 days
- mx conservative UNLESS
- Disk batteries
- > 1 magnet
- longer 5cm
- diameter >25 mm ($2 coin, other NZ coins <25mm)
- weekly radiographs if not seen to pass objects
- immediate FU if sx
Magnets
- If only ONE ingested, treat as any FB
- if >1 magnet there is risk will be in two different loops and may attach together –> necrosis, perforation, peritonitis
- -> need surgical consult
Inhaled FB
- suspect if asthma resistant to Rx and young
- On CXR can get air trapping (hyperinflation) on affected side +/- mediastinal shift
- -> if this occurs need urgent endoscopy
Button batteries
Oesophageal/nasal:
- necrosis can occur within 2 hours if touching mucosa
- -> caused by:
- electrical current
- electrolyte leakage (Na+, K+ hydroxide)
- pressure
Stomach:
- can be allowed to pass but must be followed up with radiographs to observe for disruption of the battery
- -> can cause heavy metal poisoning with mercury, silver oxide, zinc and lithium
- FU radiographs must occur in 24-48 hours
- -> if still in stomach needs endoscopic removal
Anion gap = Na+ - (Cl- + HCO3)
normal about 4-12
- normal levels albumin and phosphate needed for accurate normal anion gap
High (positive) anion gap met acidosis caused by organic acid accumulation of impaired H+ secretion: Causes (CATMUDPILES) •CO, CN •Alcoholic ketoacidosis and starvation ketoacidosis •Toluene •Metformin, Methanol •Uremia •DKA •Pyroglutamic acidosis, paracetamol, phenformin, propylene glycol, paraladehyde •Iron, Isoniazid •Lactic acidosis •Ethylene glycol •Salicylates
Normal anion gap met acidosis due to HCO3 loss:
Causes (CAGE)
•Chloride excess
•Acetazolamide/Addisons
•GI causes – diarrhea/vomiting, fistulae (pancreatic, ureters, billary, small bowel, ileostomy)
•Extra – RTA
Low anion gap met acidosis due to:
Causes
•Non random analytical errors (increased Na+, increased viscosity, iodide ingestion, increased lipids)
•Decrease in unmeasured anions (albumin, dilution)
•Increase in unmeasured cations (multimyeloma (cationic IgG paraprotein), hypercalcaemia, hypermagnesaemia, lithium OD, polymixin B)
•bromide OD (causes falsely elevated chloride measurements)
