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117 Cards in this Set
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GLobe Rupture
-suspect in ? Mx Sx |
Suspect in all cases of
-blunt and penetrating orbital trauma -high-speed projectiles with potential for ocular penetration. NOTE: You do not need to be certain the globe is ruptured – refer all patients in whom the diagnosis is suspected. Mx *Opthal referral -Avoid all pressure (extrusion), protect with a shield -do not apply drops/ointment/patch -Leave impaled objects insitu -antiemetics, analgesics, -antibiotics if delay expected -tetanus -last meal, NBM, AMPLE measure VA if possible note pupils, eye movements, haemorrhage, lacerations consider other injuries consider CT - but don't delay transfer Sx NOTE: Signs can be subtle: small lid lacerations may conceal vision-threatening globe perforations. Good visual acuity and absence of pain does not rule out globe rupture. usually: decr vision, pain, hx trauma/projectile |
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gynae emergencies
******************************** |
-ruptured ectopic
-cervical shock from retained products -ovarian cyst/mass complications eg rupture, torsion, haemorrhage |
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Acute Ureteric obstruction
cause? sx? oe? ix? |
usually due to calculus
can also be -retroperitoneal abscess/haematoma, fibrosis, malignancy sx usually unilateral flank pain+/- haematuria, fever Oe unilateral abdo/flank pain Ix basic bloods ca, uric acid MSU ?blood cultures KUB XR Non con CT urinary tract (NOT USS as obstructive signs can be delayed Mx fluid analgesia urology consult then if -obstructed kidney + sepsis ==> urgent nephrostomy or stenting -calculus with obstruction >5mm ==> surg <5mm conservative, tamulosin, surg only if FTP NOTE -never dx pyelonephritis without excluding obstruction!! |
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ECG distributions relation to coronary artery?
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PATTERNS
- anterolateral = LAD - inferior-posterior-lateral = Cx - Isolated lateral = smaller branch of LAD or LCx -inferior = RCA (80%) (can be dominant LCx) |
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ANTERIOR STEMI
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ANTERIOR STEMI = LAD
Worst prognosis due to large infarct size =ST elevation with Qwave V1-6 +/- I&AVL recipricol depression inferiorly III,AVF Different pattterns: Septal = V1-2 Anterior = V3-4 Lateral = V5-6 |
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LATERAL STEMI
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LATERAL STEMI = LAD/Cx (isolated lateral = likely branch of one of these)
ST elevation in lateral leads (I AVL, V5-6) reciprocol changes in inferior (AVF III) (NOTE if only localised to AVL & I then "high lateral") PATTERNS - anterolateral = LAD - inferior-posterior-lateral = Cx - Isolated lateral = smaller branch of LAD or Cx |
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INFERIOR STEMI
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40-50% of all MIs
more faviourable prognosis than anterior ST elevation in II, III, AVF. Progressive Qs reciprocol in AVL (+/- Lead I) 40% also have Right ventricular infarction in which pts develop severe hypotension in response to nitrates (poor prognosis) 20% develop severe bradycardia due to 2nd or 3rd degree AV block WHICH ARTERY? -80% RCA (III>II) -18% dominant LCx (III=II) -rarely wrap around LAD (concommittant anterior) |
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POSTERIOR STEMI
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Accompanies 15-20% STEMIs (usually inferior/lateral)
V1-3 changes: -horizontal ST depression -Tall broad R waves (>30ms) -Upright T waves -Dominant R wave in V2 Confirmed by ST elevation & Q waves in V7-9 REMEMBER as reflected V2 where -R =q waves depression =elevation tall t = deep TWI |
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RIGHT VENTRICULAR INfarct
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Complicates 40% of inferior stemis
Isolated very uncommon -VERY preload sensitive, can develop severe hypotension with nitrates ST ELEVATION V1 (only one that looks directly @R) ST elevation in III>II (III more right facing) ST elevation in V1>V2 (relatively) CONFIRMED with VR3-6 |
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PUPILLARY SIGNS IN HEAD INJURY
-constriction & dilation basic anatomy -signs and causes Need to complete with anatomy etc |
Dependant on
-integrity of eye/retina -optic nerve -occuolmotor, trochlear, abducens nerves & nuclei -structures surrounding nerves & nuclei REMINDER Constriction -parasympathetic --sphinter pupillae -Pathway: Edinger-Westphal nucleus near the occulomotor nerve nucleus, fibers enter the orbit with CNIII nerve fibers and ultimately synapse at the cilliary ganglion. DILATION -sympathetic -dilator pupillae -PATHWAY:begins at the cortex with the first synapse at the cilliospinal center (Budge's center) Post synaptic neurons travel down all the way through the brain stem and finally exit through the cervical sympathetic chain and the superior cervical ganglion. They synapse at the superior cervical ganglion where third-order neurons travel through the carotid plexus and enter into the orbit through the first division of the trigeminal nerve. ie Neuron1: cortex ==>budges centre NEuron2: Budges centre==>through brainstem==> cervical sympathetic chain ==> superior cervical ganglion Neuron3: cervical ganglion ==> carotid plexus ==> orbit with trigeminal I MIOSIS (Constriction) Corneal abrasion/FB interruption of sympathetic (horners) Pons intracranial haemorrhage -opioids, alcohol, neuroleptics (antipsychs) MYDRIASIS (Dilatation) Damage to sphincter Disruption of parasympathetic -3rd nerve -anticholinergics or overactivity of sympathetic -catecholamines, cocaine, amphetamines SLUGGISH PUPIL REACTIVITY -opioids, propofol, metoclopromide, haloperidol, droperidol ANISCORIA normal if <1mm difference and brisk reactions 1. Parasympathetic failure (affected pupil dilated, sluggish): look for other signs of 3rd nerve (ptosis, movements) 2. Horners (affected eye smaller) ?ptosis 3. Chemical blockade (unilateral/topical) 4. muscle damage - inflammation and trauma to the iris sphincter ?irregular IRREGULAR SHAPED PUPILS -ophthalmological procedures -muscle damage OVAL PUPILS -early compression of III (ICP) ONE EYE DOWN AND OUT -IIIrd nerve dysfunction |
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Relative Afferent Pupillary Defect
what? how? due to? |
RAPD is diagnosed by observing paradoxical dilatation when light is directly shone in the affected pupil after being shown in the healthy pupil
how swing a light between two eyes and observe reaction in both eyes due to damage in optic nerve or severe retinal disease. eg -optic neuritis -direct optic nerve damage eg trauma, tumor, radiation -severe glaucoma -ischaemia -retinal detatchment -very severe macular degeneration -retinal infection |
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Relative Afferent Pupillary Defect
what? how? due to? |
RAPD is diagnosed by observing paradoxical dilatation when light is directly shone in the affected pupil after being shown in the healthy pupil
how swing a light between two eyes and observe reaction in both eyes due to damage in optic nerve or severe retinal disease. eg -optic neuritis -direct optic nerve damage eg trauma, tumor, radiation -severe glaucoma -ischaemia -retinal detatchment -very severe macular degeneration -retinal infection |
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PHAEOCHROMOCYTOMA
what is it? What is it associated with? Clinical features Emergency complications Ix/Dx Mx Why delayed BB? |
paraganglioma -> catecholamine producing tumours
associated with: MEN, von Hippel-Lindau, neurofibromatosis and familial paragangliomas Clinical Features -paroxysmal HTN -sweating -palpitaitons -headaches COMPLICATIONS CVS - HTN crisis - shock - arrhythmia - AMI - Acute peripheral ischaemia PULMONARY - APO GIT - severe abdo pain & vomiting - acute bleed - distal bowel ischaemia due to vasoconstriction CNS - CVA, bleed, seizures PLUS renal failure, DIC Ix/Dx -SPot urine metnephrine >0.8 - increase urine and plasma catecholamines mX -Fluids -Phentolamine 2-5mg IV (pRN/infusion) -?nifedipine 10mg S/L Phenoxybenzamine 10mg BD (non specific & irreversible alpha blocker) +/- low dose beta blocker (?~2 days post alpha) Unopposed alpha ==> Beta provides some vasodilation and without it there is severe vasocontriction ==> same treatment for cocaine or other alpha stimulants (metaraminol, phenylephrine, cocaine ,amphetamines) |
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basic indications for thrombolysis?
TIme frame for thrombolysis age limit? ECG criteria? CONTRAINDICATIONs |
STEMI
haemodynamically unstable PE ISchaemic CVA AMI - 12hr ?24 hrs CVA 4.5 hrs no age limit for AMI ECG criteria -ST elevation 2mm in 2 adjacent chest leads -ST elevation 1mm in 2 adjacent limb leads -new LBBB -posterior infarction ( +ve R in V1 + -ve ST in V2) CONTRAINDICATIONS ABSOLUTE -active internal bleeding -bleeding diathesis -recent head/facial trauma, major trauma or surgery within 3 months -previous ICH -Known structural cerebral vascular lesion or malignant intracranial neoplasm -CVA within 3 months RELATIVE -Lack of verbal informed consent. -Prolonged CPR (> 10 mins)/ traumatic resuscitation -Hx poorly controlled HTN -Uncontrolled HTN at presentation: >180/110 -CVA greater than 3 months -Other intracranial disease, including dementia -DM proliferative retinopathy. -For streptokinase or anistreplase - a prior exposure (>5 days previously) or allergic reaction to these drugs -Major Surgery within 3 weeks. -Active peptic ulceration or other GI bleeding within 2-4 weeks` -Non-compressible vascular puncture/injury. -Pregnancy |
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DABIGATRAN
MOA duration? monitoring? reversal? |
competitive direct thrombin inhibitor
renally cleared after 12-14hrs APTT provides approximation of level of anticoagulation (>80s = excessive) no antidote, for bleeding: -FFP, & PRBC ?dialysis ?role of prothrombinex |
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APPROACH TO OVERDOSE
General? Charcoal? The unconcious undetermined OD |
-early mortality is low and usually relates to cardiorespiratory arrest.
-Following admission, morbidity relates primarily to aspiration pneumonitis, or a delay in definitive respiratory care. -There is a poor correlation between depth of coma and preservation of glottic reflexes. Accordingly, if there is any doubt the patient should be intubated. CHARCOAL Adequate airway reflexes must be present -if in doubt, intubate Indications If presentation <1hr from ingestion -compound bound by charcoal and ingestion expected to cause significant morbidity/mortality If presentation>1hr consider for -salicylates -slow release -agents which delay gastric emptying -drugs with enterohepatic circulation?? Charcoal is ineffective for -elemental metals & their salts -hydrocarbons, alcohols, -acids/alkilis The unconcious undetermined OD ABC(DEFG) HIstory, exam (toxidromes/trauma) Ix -basic bloods, inc paracetamol, osmoloality, ABG -ECG ?METABOLIC ACIDOSIS ?aniongap ?osmolar gap Metabolic acidosis? No - 1. Sedatives 2. Hypnotics 3. Paracetamol 4. Theoplylline 5. Anticholinergics 6. Antihistamines 7. Antipsychotics 8. Antidepressants 9. Anticonvulsants 10.Lithium 11.Organophosphates Yes Normal anion gap 1. Acid ingestion 2. Toluene sniffing 3. Bicarbonate loss Raised ANion Gap, OG<10 Salicylates Cyanide Carbon monoxide Lactic acidosis Iron Isoniazid Metformin Raised Anion Gap OG>10 Methanol, other alcohols |
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PARACETAMOL OVERDOSE
What is a potentially hepatotoxic dose in a fit adult? WHy is it toxic? Who required markedly less? How likely is survical with NAC? general approach? INdications for NAC? How dies NAC work? |
>200mg/kg or >10g (some say 150mg/kg = toxic dose)
active metabolite (NAPQI) is toxic (10-15% of paracetamol converted to this) NAPQI usually bound to glutathione, but in excess gutathione stores are overwhelmed Less required in -alcoholics -liver dz -taking cytochrome p450 inducing meds NAC 100% if within 8hrs reduced in 8-24hrs >24hrs benefit unclear APPROACH level take 4-15 hours post ingestion (if in doubt assume high risk) -plot on nomogram Pts who present >24hrs post OD with normal transaminase and unrecordable paracetamol are low risk NAC indications -<8hrs and 4-8hr level in treatment window -8-24hrshrs ->24hrs with detectable paracetamol level and elevated transaminases -unknown time of ingestion NAC Increases availability of glutathione, Directly binds to NAPQI itself Has a plasma half life of about 6hrs DETAILS/DOSAGE Dosage: 150mg/kg NAC in 200ml 5% Dex over 15 mins, then... 50mg/kg NAC in 500ml 5% Dex over 4hrs, then... 100mg/kg NAC in 1000ml 5% Dex over 16hrs The final dose is repeated until transaminases are falling and the patient is improving clinically scenarios 1. If patient presents <8hrs after a known ingestion time, NAC should be delayed until a 4hr paracetamol level is plotted on a nomogram 2. If patient presents 8-24hrs after a known ingestion time, NAC should be started and can be stopped later if nomogram shows low risk 3. If patient presents >24hrs after a known ingestion time, NAC should only be started if LFT's are deranged or paracetamol detectable 4. If ingestion time unknown, NAC is commenced |
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BILIARY GENERAL
referred pain? Causes/DDx? |
referred pain
-to right shoulder/scapula Gallstones -acute calculus cholecyctisis = obstructed cystic/bile duct +/- infection -Acute acalculous cholecystitis =inflamed gallballder in the absence of obstructio, usually in the critically ill ?ischaemic -Chronic cholecystitis =often associated with gallstones -Cholangitis =infection of the biliary system, complicating obstruction. Charcot triad = fever, RUQ pain, jaundice) Primary Biliary Cirrhosis =autoimmune, progressive destruction of bile ductules Neoplasms -gallbladder: 54% -cholangiocarcinoma: 25% adeno of ducts -ampullary: 8% painless jaundice or acute pancreatitis BIliary tract cysts (uncommon) -cystic dilatation of the biliary tree -often associated with anomalous union of pancreatic and biliary ductal system with entry of pancreatic juice |
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STROKE
What are the 4 classifications used to describe extent of stroke? (oxford stroke classification) |
4groups:
TACI, PACI, LACI, POCI -Total anterior circulation infart -partial anterior circulation infart -lacunar infarct -posterior circulation infarct TACI large cortical stroke in middle/anterior artery Dx by all 3 of: 1. unilateral weakness of face arm and leg 2. homonymous hemianopia 3. higher cerebral dysfunction eg dyspahsia, visuospatial disorder. PACI dx = 2 of above POCI dx = one of -cerebellar or brainstem syndromes -loss of consciousness -isolate homonymous hemianopia LACI subcortical stroke due to small vessel dz Dx= 1. no evidence of higher cerebral dysfunction AND one of -unilateral weakness of face/arm/leg -pure sensory stroke -ataxic hemiparesis |
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BACK PAIN
-2 major ypes of mechanical back pain -serious DDx -red flags -physical exam -to xray or not? |
1. nerve root syndromes
-radicular pain -can be due to herniated disc & impingement, spinal stenosis, spinal degeneration, cauda equina -sharp, well localised, associated with parasthesia -straight leg +ve -sx below knee associated with impingement 2. Musculoskeletal pain syndromes -Myofascial pain is characterized by pain and tenderness over localized areas, decr ROM, often relief with stretching Serious DDx -OM -CAuda equina -malignancy inc MM -AAA RED FLAGS -systemic sx eg fever, wt loss, bowel bladder -not relieved by rest/supine, awakes from sleep/non mechanical pain -prev hx maligancy -<16 or >50 with NEW onset pain -recent serious infection/illness -longstanding steroid use physical exam -straight leg (only +ve if radiation to below the knee) -abdo -consider rectal in >50yr old men ?prostatitis Classic herniation findings at different levels At L4: Pain along the front of the leg; weak extension of the leg at the knee; sensory loss about the knee; loss of knee-jerk reflex At L5: Pain along the side of the leg; weak dorsiflexion of the foot; sensory loss in the web of the big toe; no reflexes lost At S1: Pain along the back of the leg; weak plantar flexion of the foot; sensory loss along the back of the calf and the lateral aspect of the foot; loss of ankle jerk L5 and S1: These nerve roots are involved in approximately 95% of all disc herniations. TO XRAY? - history of traumatic injury or systemic illness - suspicion of malignancy or infection. -chronic steroid use and acute onset of pain in patients older than 50 years or in the pediatric age group. -cases involve (or potentially involve) litigation or for patients seeking compensation. |
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MENINGITIS- Adult
Typical presentation? Atypical presentation subgroups? Dx? Mx/ABx? SIgns of raised ICP? LP contraindications? |
Typical presentation
-fever (75-85%) -headache (87%) -objective neck stiffness, meningism -signs of cerebral dysfunction/confusion, delirium, declining conciousness 95% have 2 of -headache, -fever, - neck stiffness, - altered mental state other: vomiting, CN palsy, kernigs (9%), papillodema (1%) ATYPICAL Elderly - lethargy, obtundation, absenceo f fever, minimal meningism Neutropenia/immunocompromised - subtle Paeds - poor feeding, irritability, N&V, fever Dx -60-90%+ve on CSF gram stain (40-60% if prior ABx) -PCR CSF Mx -CT before LP to exclude cerebral abscess subdural empyema toxoplasma encephalitis Especially in focal neurology and decr LOC NOTE does not rule out raised ICP ABx Ceftriaxone 4g (100mg/kg child) daily ADD ben pen 2.4g (60mg/kg child) IV 4hrly if immunocompromised and listeria possible (pregnant, alcoholic, >50yrs) (or in meningoccal) ADD vancomycin 1.5g IV BD if strep pneumoniae on CSF antigen or otitismedia/sinusitis or is staph aureus suspected SEE RCH guidelines for alternatives Consider giving Dexamethasone to children > 2 months of age 15 minutes prior to parenteral antibiotics or, if this is not possible, within one hour of receiving their first dose of antibiotics: 0.15mg/kg IV. Consider giving steroids at the time of lumbar puncture if the clinical suspicion of meningitis is high. fluid replacement ?intubation ?DIC ?surgery/debridement/amputation Contact tracing and prophylaxis -close household contacts/kissing = rifampicin or ceft or cipro Raised ICP -cushings triad: brady, low RR, HTN -papilloedema LP CONTRAINDICATIONS -shock -widespread rash/coagulopathy -drowsiness/imparied consciousness -raised ICP -focal neurology |
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HEADACHE
-SERIOUS -other |
SERIOUS
-meningitis -ICH/SAH -raised ICP (tumours, abcess, venous thrombosis, hydrocephalus) -malignancy -hypertensive -temporal arteritis -acute glaucoma -preeclampsia OTHER -migraine -cluster -sinusitus -tension -cervicogenic -post concussion -analgesia abuse -post ictal -post LP -tigeminal neuralgia -benign Intracranial HTN -drug induced eg vasodilators |
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BURNS
ABC considerations for burns burn classification? burns to the eye? fluids? Ix? document? |
AIRWAY & CSPINE
-big distracting injury, ensure c-spine if needed -look for singed facial hair, soot in nose/mouth, stridor, voice change -assess for neck burns/swelling BREATHING -high flow non rebreather -look for constrictived chest wall burns -?toxic gas inhalation/Carbon monoxide/cyanide CIRCULATION -ivC through unburnt skin where possible -assess for circumfrential burns -shock due to burns is uncommon early so look for another cause eg tension PTX, abdo, spinal remove all jwellery and burnt/wet clothes monitor for hypothermia BURN CLASSIFICATION *superficial *partial thickness 1. superficial dermal -moist, reddened with broken blisters, brisk cap refill 2. deep dermal - moist white slough, red mottled, sluggish cap refill *full thickness - dry, painless, whitish, absent cap refill burns to the eye -early copious irrigation with normal saline or water. fluids required if >10%, calculate from time of burn. idc if >15% or perineal Ix Hb, electrolytes, blood glucose, blood group and hold. Carboxyhaemoglobin levels (if fire in confined space). DOCUMENT Time of burn Extent - Burn diagram Depth First aid Tetanus status |
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SPINAL INJURY
Who should have C-spine precautions? How is it immobilised? What should you do if a patient in cervical spine precautions starts to vomit? How do patients with spinal injuries develop respiratory insufficiency? HYpotension in spinal cord injury? Significance of priapism in SCI? MX approach to spinal injury |
C-spine precautions in
-neck pain or neuro sx -decr LOC -significant blunt injury above the clavicles (10% of major head injuries will have a spinal injury) HArd collar does not immobilise, largely reminds health practitioners Requires either -manual immobilisation -sandbags and head tape If going to vomit? -Immediate intervention is needed: --Log roll if 4 people are available — one to hold the head, and three to perform the roll. --If insufficient numbers of people are available, tilt the bed head down so that vomit runs clear of the airway. -Further intervention: --Administer antiemetics (e.g. ondansetron 4mg IV) --Seek and treat underlying causes — patients often vomit due to pain or opioid analgesia, but it can also be a sign of worrying causes such as serious abdominal trauma, hypotension or raised intracranial pressure. RESPIRATORY INSUFFICIENCY 1. high cervical injuries may lead to local haematoma & swelling 2. C5 or higher == diaphragmatic paralysis (C3-5) 3. THoracic or higher == intercostal paralysis (T1-12) OTHER CAUSES -thoracic injuries -traumatic brain injury -Cx of treatment eg sedation, fluid overload HYPOTENSION NEurogenic shock is rare compared to hypovolaemic in trauma - find the bleed. PRIAPISM ==bad prognosis --occurs at the moment of complete motor and sensory paraplegia, it does not occur following a delay -- the presence/absence of priapism assists in determining when the complete spinal cord lesion occurred.(medicolegal) --usually settles rapidly without specific treatment being required Mx -Trauma team -remove from rigid spine board to trauma bed ASAP -PRIMARY SURVEY AND RESUS -(anything above C5 require intubation) -O2 15L, monitor for resp insufficiency -fluid, look for shock, ? NA ? atropine -neuro assessment, including priapism, anal tone - |
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DROWNING
salt vs fresh Time till irreversible brain injury? Mx Prehospital Hospital Cx to monitor for and mx? Factors/timing associated with good outcome? |
no real difference between salt/fresh water other than higher bacterial load in fresh
3-10mins till irreversible brain injury Mx Prehospital -- ABC, CPR etc +/- left lateral -- only those with RF should be give c-spine precautions -- O2 if available --remove wet clothing, blankets -- neuro Ax HOSPITAL ED --Hx - duration of subersion, water temp - time to CPR, time to ROSC/breathing - ?vomiting - PMHx - alcohol/drugs/trauma -- ABC, rewarming, O2, monitoring, Ix, ?ETT, NG --maintain BGL Cx to monitor for and Mx --ARDS ?PEEP --sepsis/pneumonia (no role for prophylactic ABx unless polluted water) --consider induced hypothermia if arrested Good outcome predictied if: -- <5mins submersion -- effective CPR within 10mins -- ROSC/breathin within 30mins -- child/infant in cold water (less predictable with adults) |
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SNAKE BITE
snake bite hotline: 1800 032 675 What does a snake bite look like? Non-specific signs of snake bite? Specific signs of snake bite? FIrst aid mx? ED Mx? Antivenom administration? LAte complication? interest: Difference between venomous and poisonous |
--most venom reaches blood vialymphatic system
BITE -the bite may be painless, there may be no puncture marks or paired fang marks. there may be just a single mark or scratch Non-specific signs -N&V&D, abdopain -headache, dizziness -sweating Specific signs -swollen, tender lymph nodes draining the bite -cranial nerve palsy, blurred/double vision -limb weakness or paralysis -respiratory weakness or arrest -drooling, difficulty speaking, swallowing -coagulopathy -rhabdo (myalgia, weakness, CK>1000) FIRST AID immobilisation & pressure bandage -do not wash bite site ED Resus (ABC/CPR) IV access monitoring assess for coag, paralysis (ptosis) IX - bloods inc coags & CK, blood grouping consider - haemolysis screen (haptoglobin, LDH, bloodfilm) urinalysis for myoglobinaemia (blood on dip) -venom detection kit if no signs or sx -remove bandage slowly!! -continue monitoring -lab tests 1hr after bandage removal then 6 and 12 hrs -carefully assess for ptosis if signs and symptoms -venom detection kit inconclusive then give polyvalent anti venom (have adrenaline ready) -venom kit conclusive give appropriate -manage in ICU ?dialysis -FFP may be required depending on fibrinogen/haemorrhage Antivenom administration -infusion in 20-30mins -have adrenaline ready (IM), ensure working 2 IV lines -if known previous reaction to antivenom give steroid and administer infusion slowly -if reaction, stop infusion, treat and then restart -some pts may require multiple doses LAte complication -serum sickness, 5-10 days post antivenom ==> fever, rash arthralgia, myalgia INTEREST If it bites you and it makes you sick - venomous If you bite it and it makes you sick - poisonous antivenom made from horse serum |
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NOF fracture
types? Mx? |
Classifications
-complete/incomplete -displaced? non displaced? -intracapsular/trochanteric OR subcapital/intertrochanteric/subtrochanteric Mx ABC/resus ?dehydration Analgesia ?early nerve block if pt in severe pain IDC NBM Xmatch/bloods ?IVF ECG CXR usual meds |
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AORTIC DISSECTION
Types/classification? Risk factors Sx/Sx Arteries that cane be effected |
Classification
Proximal/A - ascending aorta involved - sub classification - arch involvement Distal/B - decending aorta only RF • Congenital cardiovascular disease • Bicuspid aortic valve disease or coarctation • Connective tissue disease Marfan’s syndrome or Ehlers-Danlos syndrome • Hypertension • Cocaine use • Pregnancy • Thoracic trauma • Recent invasive medical or surgical procedures Sx/Sx • HTN • Restlessness • Unequal blood pressure in both arms • Absence of/changes in peripheral pulses • Pallor • New diastolic murmur of aortic insufficiency • Symptoms of shock indicative of rapid progression or possible rupture of dissection ~ Tachycardia ~ Hypotension ~ Oliguria ~ Diaphoresis ARTERIES • Brachiocephalic Artery -peripheral pulses • Coronary Artery Obstruction -Chest pain, ECG • Renal Artery Obstruction -Decreased urine output • Carotid Artery -LOC, syncope, dizziness, paralysis. • Superior Mesenteric Artery Obstruction Increased bowel sounds, maelena, abdominal pain. • Iliac Artery Obstruction- peripheral pulses. |
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RED EYE
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PAINLESS (rarely requires urgent ophthal Ax)
Diffuse: -conjunctivitis, -blepharitis(non-specific generalised lid inflammation) -ectropion (lids turning outwards) -trichiasis (mis direction of eyelids towards the globe) -eyelid lesion Localised: -corneal foreign body (remove, top Abx) -ocular trauma -subconjuctival haemorrhage (BP, coags, vision) -pterygium PAINFUL Cornea abnormal: -herpes simplex(topical acyclovir) -bacterial/acanthamoebal ulcer** urgent referral, usually contact lense wearer) -marginal keratitis* discuss -FB/corneal abrasion Lids Abnormal: -chalzion -blepharitis -herpes zoster Diffusion conjunctival injection -viral conjunctivits *highly contagious, see below -allergic conjuntivitis -bacterial conjuntivitis -dry eyes Other -closed angle glaucoma*** hazy cornea, irregular semidilated pupil, shallow anterior chamber, eyes is very tender/tense, headahce/N&V -cilary injection/scleral involvement**** -anterior chamber involvement**** eg acute uveitis/iritis:pain, photophobia hypopyon hyphema NOTE refer viral conjunctivitis if: -Photophobia & marked decrease in visual acuity -severe dz requiring steroids -lasting >3 weeks ?chlamydia, other -Work cover issues |
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cspine clearance
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-need to be done within 72 hours due to collar ulcers
-awake and alert pts may be cleared by exam and history (Level1 evidence) -in the obtunded pt CT is sufficient to clear -CT of occiput to T1 is required |
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?use of factor VIIa in trauma
in liverpool requires haematological approval criteria |
-consider in blunt penetrating trauma with refractory bleeding
-do not use in crush injuries or brain injury -do not use in hx thromboembolic/atherosclerosis -90mcg/kg (round down to nearest 1000) IV over 2-5mins liverpool criteria for the use of recombinant Factor VIIa • Bleeding continues despite conventional therapy • All attempts to control bleeding by surgery or embolisation have been taken, and • In general: at least 10 units of red cells, 2 pooled platelets, 10 FFP and 10 units of cryoprecipitate have been given and • The Specialist has consulted the Haematologist on call and they agree that the coagulopathy cannot be otherwise corrected |
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Criteria for paging trauma team
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Mechanism
• MVA ejected from vehicle • Pedal cyclist, motorcyclist or pedestrian hit by car or truck • Fall 6m or greater • MVA with one or more fatality • Fall from horse • Interhospital trauma transfer Vital Signs • Airway obstruction • Shallow or retractive breathing • Cyanosis • Skin pallor or slow capillary refill >2 sec. • Systolic blood pressure <90 mm/Hg • Pulse >130 or <50/min • Depressed level of consciousness or fitting • Pupil(s) dilated or unreactive • Trauma Score 12 or less • Deterioration in Emergency Injuries • Injuries to 2 or more body regions (head / neck / chest / abdomen / pelvis / back / femur) • Fracture to 2 or more long bones (adjacent radius/ulna or tib/fib do not count as 2) • Spinal cord injury • Crush injury or amputation of a limb • Penetrating injury to head, neck chest, abdomen, pelvis, groin or back • Burns to airway or smoke inhalation. Adults >15% surface area, children >10% |
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size of a large bore chest drain?
small bore? which size to use for what? macgyver chest drain valves? |
large bore = >20Fr
Small bore <=16F Blunt dissection PTX: 20-24Fr (6.7-8mm) Effusion/Pus: 20-28Fr (6.7-9.3) Blood: 32Fr (10.7mm) Situations where insertion of a large bore chest tube by blunt dissection may be indicated include: -traumatic haemothorax, especially if haemodynamic instability is present -tension pneumothorax or a large pneumothorax with anticipated high flow air leak, especially in the post surgical context. Small bore catheters are recommended as first line therapy for pneumothorax, free flowing pleural effusions and pleural infections. NOTE (Use a 25 G needle to raise a dermal bleb then use a 21G needle to infiltrate the skin, subcutaneous tissue, muscle, periosteum and the parietal pleura) macgyver chest drain valves -glove with a finger cut off -most medical drainage bags have a one way valve to prevent reflux |
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hypothermia
defined as? Effects? Treatment? |
<35, severe <28
CVS: -decr CO & MAP, -ECG wide QRS , incr PR, Jwaves, -incr viscosity & myocardial work -risk of VF <28 GIT -decr liver metabolism * circulation -decr splanchnic circulation METABOLIC -left shift oxyHb curve, -hyperglycaemia, -decr drug metabolism NEURO -neuroprotection -fixed dilated pupils <30 HAEM -incr bleeding time -incr VTE risk RENAL -decr GFR & RBF, poly uria NOTE Labs may not be reliable due to temp TREATMENT -prevent further heat loss & rewarming (remove wet clothe, add blankets, active warming groin axilla abdo- careful of burns, warmed fluids -ETT -mx arrhythmias (cardiac pacing and atropine are generally ineffective for brady arrhythmias, lidocaine is ineffective for arrythmias) -volume resus, inotrope |
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sudden vision loss
(CIAP emergency EYE manual) |
TRANSIENT
Transient Ischaemic Attack (Amaurosis Fugax) -monocular -usually secs to mins, can be 1-2hrs -vision returns to normal PERMANENT -urgent ophthal *Central Retinal Vein Occlusion (CRVO) -sudden, painless *Central Retinal Artery Occlusion -sudden, painless -urgent ESR/CRP to exclude GCA *Optic neuritis -painless over hours to days ArteriticIschaemic Optic Neuropathy(AION)/Giant Cell Arteritis (GCA) -temporal headache, scalp tenderness, jaw claudication, generalised muscle aches/sweats -urgent ESR/CRP Retinal Detachment. -painless, ?increased floaters -minimise activity, bed rest |
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dizziness
-approach? |
-need to differentiate a central serious cause from a benign peripheral
central - 85% vascular 10% demyelination peripheral - BPPV, vestibular neuritis, menieres Suggestive of stroke: -multiple prodromes -recent trauma -"hard" neuro signs like CN palsy -normal head impulse test if continuous vertigo then do HINTS Head Impulse test NORMAL Nystagmus (direction changing or vertical/tprsional) Test of Skew (vertical ocular misalignment, cover eyes altnernately to see skewed eye move) ** if any one one of 3 abnormal 100% sensitivity 85% specificity for central cause NOT HELPFUL -differentiating type of dizziness -gradual vs sudden onset -hall pike -severity of sx -hearing loss -CT http://academiclifeinem.blogspot.com.au/2011/12/paucis-verbis-acute-vestibular-syndrome.html |
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febrile neutropenia
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diarrhoea
kids -best measure of dehydration -when to use IV fluid vs oral/NGT? -when to collect/culture stool? general DDx |
Cap refill
tugor RR IV fluid therapy if -shock -dedterioration despite oral therapy -persistant vomiting of oral fluids Stool culture if -?sepsis -immunocompromised -blood/mucous -abc -20ml/kg -keep warm DDx INFLAMMATORY infective - cdiff, salmonella shigella etc IBD radiation ischaemic colitis SECRETORY toxins, endocrin, neoplastic, drugs INCR MOTILITY drugs OSMOTIC malabsorption, laxatives, |
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Nausea and vomiting adults & kids
DDX wikem has good ddx list |
-DKA & other endocrine
CNS -head injury, meningitis, cva, raised ICP GIT -gastro -obstruction eg pyloric stenosis, insussuseption, volvulous, hernis -appendicitis, cholecystitis, pancreatitis, hpeatitis -mensteric ischaemia infectious eg UTI drugs pain eg torsion |
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testicular pain
DDX? Sx assoiciated with torsion? Dx? Manual detorsion? |
-torsion
-epididymitis -hydrocoele -hernia/kidney stones -epididymal torsion -mumps -scrotal mass/tumour -varicoele -spermatocoele -fournier gangrene/necrotising infection of perineum Sx assoiciated with torsion? -Pain duration of less than 24 hours -Nausea or vomiting -High position of the testicle -Transverse lie of the affected testis -Abnormal cremasteric reflex Dx -Imaging studies (eg, USS) may be useful when a low suspicion of testicular torsion is noted -Surgical exploration should not be delayed for the sake of performing imaging studies. MANUAL DETORSION - not recommended if >6hrs -"opening a book" eg twisting outward and laterally -Rotation of the testicle may need to be repeated 2-3 times for complete detorsion. -Pain relief serves as a guide to successful detorsion, but restoration of blood flow must be confirmed -Other signs suggestive of successful manual detorsion include resolution of the transverse lie of the testis to a longitudinal orientation, lower position of the testis in the scrotum, and return of normal arterial pulsations detected with a Doppler stethoscope ?elective orchiopexy to prevent further |
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haematesis/GIT bleed
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vaginal bleeding
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intermenstual
-post coital -ca -vaginitis -thyroid -ectopic -infection -hyperprolactinaemia mx pap smear pregnancy trest bloods including coagss and tft ?USS -if >40 for hysteroscopy post menopausal -refer very heavy menstrual bleeding oral progestagens -a regime of norethisterone at a dose of 30mg per day is inititated (which is generally effective within 24-48 h); the dose can then be reduced by 5mg per day and then stopped. This regime will be followed by a withdrawal bleed The cause for the heavy menstrual bleeding must be investigated. |
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haemoptysis
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massive - abc. urgent pulm consult +/- cardiothoracics
non-massive -?non-lower respiratory cause eg sinusitis, epistaxis, git -cxr +/- HRCT -bronchoscopy if non diagnostic ct or recurrent bloods abg, d-dimer, coags, ?esr sputum ddx non-resp -nasopharyngeal -git common -infection (acute bronchitis(26%), pneumonia(10%), tb,,, -lung ca less common -cardiovascular (PE, AVM, CHF) -pulm (FB/trauma, bronchiectasis, abcess, good pastures, wegners, lupus) |
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sore throat
see sore throat guideline RCH |
DDX
-viral URTI -EBV -Group A strep -<4yrs probably viral -features of viral urti: cough, coryza, conjunctivitis= probably viral fever+malaisgeneralised lymphadenopathy/splenomegaly ==> EBV fever+ pharyngotonsilitis+tender tonsillar lymph nodes ==> throat swab & ABx, r/v culture in 48hrs to determine whether to continure ABx |
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fracture management
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pericarditis
sx ECG changes iX |
chest pain, pericardial rub & serial ECG changes
-retrosternal chest pain with referrral to trap ridge, neck, L shoulder/arm -better sitting up -can also have low grade fever, cough +/- tamponade sx ECG widespread ST elevation PR depression/elevation normalised then diFFUSE twI iX ECG cxr BLOODS INC crp tni ldh ?echo Mx NSAID 7-14 days reasons to consider admission -fever> (38°C), -subacute onset, -immunosuppression, -trauma, -oral anticoagulation therapy, -aspirin or nonsteroidal anti-inflammatory drug (NSAID) -treatment failure, -myopericarditis, -severe pericardial effusion, -cardiac tamponade |
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rhabdo
-what is it? -what causes it? -Dx? -what does it lead to? Mx? |
- clinical syndrome caused by
insults to myocytes and muscle membranes that lead to the destruction of skeletal muscle and release of muscle fiber contents into the bloodstream. CAUSED BY -direct muscle trauma (most common) -genetic enzyme deficiencies -toxins/drugs -infections -endocrine eg DKA, HONK, hypothyroid Dx best way through CK >5000 (assuming no cardiac/brain issues) clincal syndrome muscle aches pain, weakness, tea coloured urine -electrolyte disturbance -renal failure 2ndry myoglonuria -DIC NOTE Grossly visible myoglobinuria does not manifest until at least 100 g of muscle is destroyed; thus, early measurement of serum and urine myoglobin is essential Mx -resus, aggressive fluid replacement -manage electrolytes (Don't giv Ca unless symptomatic) -?haemodialysis ?urinary alkinisation -avoid nephrotoxins |
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bowel obstruction
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STIs
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osteomyelitis
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toxidromes
-TCAs -seretonin syndrome neuroleptic malgnant syndrome |
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procedural sedation
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biers block
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GOUT
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hepatitis
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heart failure
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thyroid disease, storm
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otitis media
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neonates
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pregnancy complications
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abruption
preavia prolapse.... hyperemesis bleeding pain pre/eclampsia |
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mental health in emergency
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carbon monoxide toxicity
-toxic mechanism? -clinical features? -Dx? -Mx? |
x210 affinity for Hb than O2, binds to one of 4 binding sites which massively increases O2 binding affinity hence decreased O2 unloading to tissue
(also othermechanisms: -affects mitochondria function further exacerbating tissue hypoxia -causes endothelial release of oxygen free radicals) all leads to dymyelination of white matter and delayed brain damage Clinical Features: -Headache, nausea, dizziness, confusion, seizures & coma -Tachycardia & hypertension, Ischaemic ECG changes -Non-cardiogenic pulmonary oedema -Lactic acidosis -DIC - Due to endothelial damage Dx -sats are useless -carboxyhaemaglobin level Whatever this value is, subtract from recorded sats to give you the maximum possible sats value <10% Normal in a smoker 10% Slight headache 20% Dizziness, nausea, severe headache 30% Ataxia, visual disturbance 40% Confusion, coma, seizures, syncope 50% Cardiorespiratory collapse, seizures Management: 100% oxygen ASAP until all Sx resolved & COHb normal If severe transfer to hyperbaric unit, pregnant patients should receive this |
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miscarriage
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THREATENED
Advise a woman with vaginal bleeding and a confirmed intrauterine pregnancy with a fetal heartbeat that: -if her bleeding gets worse, or persists beyond 14 days, she should return for further assessment -if the bleeding stops, she should start or continue routine antenatal care. CONFIRMED MISCARRIAGE Expectant management vs Medical management vs suRGICAL Expectant(7-14days) not suitable if: -incr haemorrhage risk eg late 1st trimester -previous adverse trauamtic pregnancy -evidence of infection -information, advice on pain relief -urine pregnancy test after 3 weeks Medical vaginal misprostal (oral if this not possible) pain relief & antiemetics Surgical -manual vacuum under local -surgical under GA |
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paediatric airway/resp ddx
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bronchiolitis (cause of most <2)
-RSV usually, can be adenovirus, infulenza, parainfluenza -croup -bacterial tracheitis -foreign body -retropharyngeal abcess -epiglottitis -asthma Hx fever choking trauma other illness |
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bronchiolitis
what is it? Time course? Risk factorsfor severe bronchiolitis? examination features? iX Mx when to consider paeds consult? see RCH |
- viral lower respiratory tract infection, generally affecting children under 12 months of age.
-After 12 months of age consider overlap with asthma. Peak severity is usually at around day 2-3 of the illness with resolution over 7-10 days. The cough may persist for weeks. RF Young, especially < 6weeks Ex-premature infants Congenital Heart disease Neurological conditions Chronic respiratory illness Pulmonary hypertension EXAMINATION FEATURES - increased work of breathing (link) - widespread wheeze and crepitations - +/- fever - May have reduced oxygen saturation - Look for signs of dehydration Ix none usually required CXR if diagnostic uncertaininty Mx -supportive -minimal handling -oxygenation and hydration -smaller feeds -can trial salbutamol but no evidence consider paeds consult if - Discharged prior to day 3 of illness with other risk factors (see history). - Abnormal oxygen saturations - Less than half normal oral intake or urine output - Assessed as moderate or severe bronchiolitis |
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HSV vs HZV vs shingles vs varicella vs chickenpox etc
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THere are 8 herpes viruses
One of them is Varicella zoster virus (VZV) Causes -Chickenpox in children -herpes zoster (shingles) in adults Another is Herpes simples virus (HSV) -HSV 1generally causes cold sores -HSV 2 generally causes genital herpes |
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TORTICOLLIS
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Torticollis is not a diagnosis but a symptom of diverse conditions.
Torticollis results in a fixed or dynamic posturing of the head and neck in tilt, rotation, and flexion Spasms of the -sternocleidomastoid, -trapezius, and -other neck muscles, usually more prominent on one side than the other, cause turning or tipping of the head congential (RARE) VS acquired CONGENTITAL -birth trauma -intrauterine malposition ACQUIRED -injury or inflammation of the cervical muscles or cranial nerves eg blunt trauma, antipsychotics, atlanto axial subluxation |
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CSF DIFFERENTIAL
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WBC
SHould have 5 or less and be mononuclear virus = increased lymphocytes bacterial & fungal = incr PMN (neutrophils) GLUCOSE = 60% of serum PROTEIN = 1/200 serum protein NOTE xanthrochroma will peak at 48hrs post bleed, can persist 2-4weeks ?RBC to WBC ~8000 |
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paediatric sepsis antibiotic guidlines
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SEE RCH ANTIBIOTIC GUIDLEINES
Sepsis -with unknown CSF Fluclox 50mg/kg (2g) IV Q4hr AND cefotaxime 50mg/kg (2g) iv Q6hr (if CVL or ?MRSA -replace fluclox with vanc 15mg/kg (500mg) IV Q6hrs -with normal CSF gent replaces cefotaxime 7.5mg/kg (360mg)IV daily FEBRILE NEUTROPENIA (see rch guidelines) cultures then ABx within 1hr Piptaz +/- amikacin+/- vancomycin piptaz 100mg/kg (4g) IV Q6hr amikacin 22.6 mg/kg (1.5) IV Q24hrs vanc 15 mg/kg (max 500 mg) iv 6H |
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neonatal ddx
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SEPSIS
-CNS, pulm, UTI -consider GBS status and neonatal herpes HEART DISEASE -acyanotic eg closure of DA ?hepatomegaly/HF also: AS, coarctation, PDA, VSD, ...lots ?PGE 0.05 mg/kg IV then infusion of 0.05 to 0.1 mg/kg /min IV ? frusemide -cyanotic 6 causes (present within 2-3weeks when DA closes) 1. transposition of GV 2. total anomalous pulm venous return 3. terology of fallot 4. truncus arteriosus 5. tricuspid atresia 6. severe pulmonic stenosis PGE as above Age-appropriate airway equipment should be available before starting PGE1-non-dose-dependent side effect: apnea TRAUMA -NAI/accidental ENDOCRINE -CAH, thyrotoxicosis (CAH 25-50mg/m2 hydrocort) METABOLIC -electrolytes -Inborn errors of metabolism INTESTINAL CATASTROPHIES -volvulus, intersusseption, necrotising enterocolitis TOXINS/POISONS SEIZURES -abnormal eye movement (usually horizontal, sustained deviation), lip smacking, abnormal tongue movements, pedaling, or apnea -hypoxic, ischaemic, infective, glucose...many |
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abdominal/pelvis trauma
-common injuries to keep in mind |
abdo - bowel vessel disruption==> bowel ischaemia
pelvic - bleeding, usually venous -urethral injury spinal - chance fracture lumbar (lap belt) +/- pancratic/duodenal injuries aorta & vessels solid organs (particularly if lower rib #) -spleen -liver -kidneys (frank haematuria) FAST scan common dependent fluid collections -between spleen/diaphragm & spleenkidney -liver/kidney Morrison's pouch -pelvis CT |
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FAST SCAN
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FAST scan common dependent fluid collections
-between spleen/diaphragm & spleenkidney -liver/kidney Morrison's pouch -pelvis |
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chance fracture
-what is it -who gets it/mechanism -what other injury is often associated with it? -what do you see radiologically -tx? |
Chance fractures are hyperflexion injuries in which there is distraction of the posterior elements and impaction of the anterior components of the spine
o Compression component from hyperflexion is usually minor compared to distraction component Originally most often caused by seat belts as hyperflexion injuries in automobile accidents o With lap belts, it is now seen more often with falls Up to 50% of individuals with Chance fractures may also have serious blunt injury to internal organs § Injuries involve primarily the pancreas, duodenum and mesentery Horizontal fracture through the spinous process, laminae, pedicles and vertebral body Most are managed with immobilization o Instability is frequently associated with a kyphosis of 20° or more and a kyphosis of 30° or more usually requires internal stabilization |
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chest trauma
What immediately life-threatening chest injuries should be considered during the primary survey of major trauma patients? other injuries? |
-airway obstruction/damage
-tension PTX -open ptx -massive haemothorax -flail chest -tamponade -aortic dissection/injury chest wall injury - causes respiratory compromise, bleeding, ? force transmission -difficult to fracture/dislocate posterior ribs, more commonly lateral cardiac -contusion -mediastinum lungs -PTX -contusion -haemorrhage great vessels oesophagus |
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flail chest
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-paradoxical chest movement
-unable to genrate -ve intrathoracic pressure hence requires positive pressure ventilation (BVM or intubation) |
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paediatric wt estimation equation
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wt = (age+4)*2
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signs of major airway obstruction or disruption? (trauma setting)
if laryngeal injury suspected - Mx? |
-External neck deformity or hematoma, crepitus from laryngeal fracture, surgical emphysema, hoarse voice or gurgling
-Complete airway obstruction — silent chest, paradoxical chest movements -Partial airway obstruction — stridor, respiratory distress -Cyanosis LAryngeal injury -high flow O2 -airway maneurvers and adjuncts -definitive airway BUT intubation can be hazardous -can worsen preexisting injury, further tears or cricotracheal separation -also anatomy may be distorted SIMILARLY cricothyroidotomies not ideal IDEALLY tracheostomy under local Unstable –– Tracheotomy and neck exploration Stable patients –– Flexible fiberoptic laryngoscopy in the ER CT scan, direct laryngoscopy, , bronchoscopy and esophagosopy don't probe open wounds - can dislodge haematoma CT scan - evaluation of laryngeal skeletal framework -non-invasive |
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blunt and penetrating neck injury-what are your primary areas of anatomy that you are intially worried about.
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-airway
-major vascular structures -cervical oesophagus -cervical spine |
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massive haemothorax
-when is thoracotomy indicated? -Mx |
-Blood loss > 1,500 mL or 1/3rd of blood volume
-Blood loss >200 mL/h (3 mL/kg/h) for 2-4 hours -High flow oxygen 15L/min via non-rebreather -Treat with rapid restoration of blood volume combined with concurrent drainage of thorax -Immediate intercostal catheter insertion (re-expanding lung may tamponade the bleeding vessels) -Hemostatic resuscitation — activate massive transfusion protocol, use of an autotransfuser is ideal -Thoracotomy |
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METHODS WHICH DECREASE ABSORPTION AND ENHANCE DRUG ELIMINATION
charcoal -how does it work? -when do you use it Gastric lavage Haemodialysis -when used ? |
CHARCOAL
Directly chelates toxic substances (Also reduces enterohepatic circulation so reducing toxic agent bioavailabitlity) eg barbiturates / tricyclic antidepressants Best if given within 1-4hours of toxin ingestion Note patency of airway is essential LAVAGE -rarely used, can be used for slow release meds -if used <1ml/kg exchange volume HAEMODIALYSIS -severe intoxication of salicylates, lithium, alcohols, metformin, etc |
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Salicylate toxicity
-toxic dose? -toxic mechanism? -metabolised by? -Elimination half life? -Mx? |
Threshold toxic dose tends to be >150mg/kg (10g) in a normal adult (same as paracetamol)
-Irreversible inhibition of COX enzymes ==> decr PG synthesis -salicylates directly stimulate respiratory centre causing hyperventilation -inhibit anaerobic respiration ==> lactic acidosis metabolised by liver elimination half life 2-4 hrs (untreated) Mx -there is no antidote -ABC -Administer activated charcoal orally (50g), can be repeated 4hrs later if serum levels continue to rise -Urinary Alkalinisation: Increases the pH of the urine This promotes the ionisation of highly acidic drugs (like salicylates) 1-2mmol/kg of Sodium Bicarbonate is given as a bolus Followed by 100mmol in 1L Dextrose at 250ml/hr Aim for a urinary pH of >7.5 Continue until patient stabilising and labs normalising Renal replacement therapy may be used if toxicity is very severe or urinary alkalinisation is unfeasible (Eg: Underlying renal failure |
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methanol poisoning (found in paintthinner)
-MOA? -clinical features? |
toxic/lethal dose =0.5ml/kg
MOA toxic metabolites Metabolised in the liver to formaldehyde ==> formic acid Formic acid affects mitochondria, causes cellular hypoxia at the molecular level Clinical Features: -CNS depression (like EtOH) - severe metabolic acidosis with raised anion gap -Osmolar gap also raised, due to osmotic effect -Retinal oedema (blindness) & cerebral oedema (seizures) Mx -intubation -for CNS depression & acidosis -bicarbonate (aim pH >7.3) -renal replacement = the definitive mx, removes methanol and formic acid -antidote = ethanol (competes for alcohol dehydrogenase, 20x greater affinity) NOTE Ethylyne glycol very similar sx& mx (antifreeze, brake fluid) |
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LAryngo tracheal injury classification
Mx for each |
Group I injuries
–– No fracture –– Minor hematoma, edema or laceration Group II injuries –– Nondisplaced fractures –– Edema or hematoma –– Minor mucosal disruption without exposed cartilage Group III injuries –– Displaced fractures –– Massive edema or mucosal disruption –– Exposed cartilage and/or cord immobility Group IV injury (group III) –– Addition of two or more fracture lines –– Skeletal instability or significant anterior commissure trauma –– Complete laryngotracheal separation Group1 –– Minimum of 24 hours of close observation –– Head of bed elevation –– Voice rest –– Humidified air –– Anti reflux medication –– Serial flexible fiberoptic exams --Antibiotics for laryngeal mucosa disruption Group II-V require surgical intervention -Hemostasis -Evacuation of hematoma -Reconstruction of the laryngeal framework -Coverage of de--epithelialized surfaces Surgical options –– Endoscopy alone –– Endoscopy with exploration –– Endoscopy with exploration and stenting |
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flail chest
-recognigtion -managment |
Recognition
-Chest pain -Respiratory distress -Boney crepitus -Paradoxical chest wall movements of the affected segment (not apparent if positive pressure ventilation applied) Management -High flow oxygen 15L/min via non-rebreather -Analgesia — paracetamol 1g qid po, NSAIDs if not contraindicated, titrated opiates IV (e.g. fentanyl 25 micrograms q5min prn IV). Early use of regional anesthesia (intercostal nerve blocks, paravertebral block, epidural anesthesia) due to risk of respiratory depression. -Respiratory monitoring and support — close monitoring of SaO2, respiratory effort, and ABGs is important as patients tend to gradually deteriorate and may require intubation and mechanical ventilation. |
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tamponade
-most likely situation/mechanism -amount of fluid needed to tamponade -recognition -management |
Pericardial tamponade is more common in penetrating thoracic trauma than blunt trauma.
As little as 75 mL of blood accumulating in the pericardial space acutely can impair cardiac filling, resulting in tamponade and obstructive shock. Recognition -Anxiety and agitation -Obstructive shock — tachycardia, hypotension, cool peripheries -Beck’s triad: muffled heart sounds, hypotension and distended neck veins — not especially in a noisy trauma bay! -Pulsus paradoxus (drop in systolic blood pressure >10 mmHg on inspiration) -Very hard to differentiate clinically from tension pneumothorax and needs to be actively sought Mostly diagnosed following identification of a pericardial effusion on bedside ultrasound as part of the FAST exam ((see hemopericardium at ultrasoundvillage.com) Management -High flow oxygen 15L/min via non-rebreather -May transiently respond to fluid challenge -Needle pericardiocentesis, preferably ultrasound guided, -Pericardotomy is definitive treatment |
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organophosphate poisoning (agricultural insecticides)
-toxic mechanism -toxicokinetics -clincal effects -Dx? -mx |
TOXIC MECHANISM
-binds Acetylcholinesterase preventing ACh binding -incr ACh at both muscarinic & nictotinic -after a period of time bond becomes irreversible and antidote does not work TOXICOKINETICS -extremely well absorbed via all routes, inc transdermally -a spoon ful is lethal -half life >100hrs CLINICAL EFFECTS -variable, onset may take hours -cholinergic syndrome: Acute Muscarinic Effects -Diarrhoea, urination, lacrimation, salivation, bonchorrhoea& bronchospasm, emesis -miosis, --ve chronotropy, inotropy -vasodilation (M3) -sweating (although usually sympathetic, driven by muscarinic) Acute Nicotinic Effects -depolarising neuromuscular blockade due to constant stimulation of motor endplate, similar to sux Dx -often clinical (pts often stink of garlic) -LAb - Red cell cholinesterase levels & plasma butyrylesterase (pseudocholinesterase) levels, toxic effects if these are <25% normal Mx -PPI, -ve pressure isolation -Atropine (indicated if severe eg bradycardia, 1.2mg) double dose every 5 mins until sx improve, doses of up to 100mg may be needed, ongoing infusion is usually necessary -therapeutic endpoint is drying of secretions -ANtidote: Pralidoxime. prompt administration critical before bonding occurs. 30mg/kg over 15min loading dose 8mg/kg/hr maintenance (inchildren 15mg/kg/hr) |
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cyanide poisoning
-toxic mechanism -mx |
Binds to the ferric Fe3+ ion of cytochrome oxidase
-causes tissue hypoxia ==> lactic acidosis CNS: triggers release of neurotransmitters esp NMDA causing seizures, LOC Pulm & coronary vasoconstriction elimination half life 2-3 hrs Mx antidote: Dicobalt edetate or Hydroxocobalamin effectively chelate cyanide Must be given early though |
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Neuroleptic malignant syndrome
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Seritonin syndrome
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tricyclic overdose
?potential life threats? -TOxic mechanism -life threatening dose -clinical manifestation of large dose? -ECG findings -antidote? indications? |
coma
respiratory acidosis seizures cardiac dysrhythmia cardiac arrest NOTE type 1a antiarrhythmics amiodarone, and beta-blockers are contra-indicated. treat with NA Bicarb -noradrenaline and serotonin reuptake inhibitors - GABA-A receptor blockers. -Cardiotoxic effects primarily result from blockade of inactivated fast sodium channels = life threatening dysrhytmias, myocardial depression Life threatening dose ->10mg/kg, >30mg/kg = severe toxicity with pH dependant cardiotoxicity and coma >24hrs rapid deterioration within 1-2 hours of ingestion – even if the patient is alert with a normal ECG on arrival. (Delayed effects may result from anticholinergic-mediated delayed gastric emptying or extended release amitriptyline.) *CNS sedation and coma tend to precede cardiotoxicity seizures delirium (anticholinergic) *cardiovascular sinus tachycardia and possible mild HTN initially hypotension (alpha-blocking effects and myocardial depression) broad complex tacydysrrhythmia broad complex bradycardia occurs pre-arrest *anticholinergic effects may occur on presentation or may be delayed and prolonged agitation, restlessness, delirium mydriasis dry, warm flushed skin urinary retention tachycardia ileus myoclonic jerks ECG -QRS widening -RAD Antidote - Sodium biacrb 50 mmol/50 mL (mechansim multifactorial & poorly understood) 100 mmol (2 mmmol/kg) bolus every few minutes while monitoring the effect on ECG until haemodynamically stable indications -severe cardiotoxicity (arrest, ventricular dysrythmia, hypotension resistant to fluid -risk of acidosis eg seizure, prolonged intubation attempt |
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acute dystonic reaction
-most common cause? -sx? underlying pathophysiology? Mx? ?discharge |
usually caused by reaction to haliperidol - torticollis
90% occur within 5 days of starting antipsychotic (can also be caused by antiemetics, ssris, ABx, anticonvulsants.....) Dystonia refers to sustained muscle contractions, frequently causing -twisting, -repetitive movements or -abnormal postures. They may affect any part of the body. Patients are often frightened and fearful, and may be in considerable pain. Mental status is generally unaffected, anxiety & agitation are common Specific presentations layryngeal dystonia — rare but potentially life-threatening Oculogyric crisis — rotatory eye movements or deviated gaze Blepharospasm and other facial spasms — spasm of the eyelids (unable to open eyes) or other facial muscles Buccolingual crisis — protruding or pulling sensation of the tongue Torticollis, antecollis or retrocollis Torticopelvic crisis — abdominal rigidity and pain Scoliosis or lordosis — lateral flexion of the spine or extension. Opisthotonic crisis — spasm of the entire body characterised by back arching, flexion of the upper limbs and extension of the lower limbs. underlying pathophysiology - imbalance of dopaminergic and cholinergic neurotransmission Mx -ABC -Benztropine (5-20mins), can give 2nd dose after 30mins, then ?DDx. 1-2mg IV (0.02mg/kg max 1mg for paeds) [anticholinergic] -2nd line = benzos -3rd line antihistamine (H1 antagonist) if no airway/resp compromise/sx can d/c home with 3 days of benztropine 1-2mg BD |
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acute coronary syndrome
Risk stratification Mx |
RISK
TIMI (0-5) or pretest ACS LOW -MED RISK - ?STRESS TEST monitoring O2 aspirin 300mg clopidogrel 300mg clexane statin beta blocker (if no hypotension, brady, APO) |
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haemolytic uraemic syndrome
describe DDX Mx |
progressive renal failure that is associated with microangiopathic (nonimmune, Coombs-negative) hemolytic anemia and thrombocytopenia.
==>thrombotic microangiopathies the most common cause of acute renal failure in children (can occur in adults too) TYPES Typical HUS (Shiga-like toxin–associated HUS) Aypical HUS (nonShiga-like toxin–associated HUS) ddx Antiphospholipid antibody syndrome Malignant hypertension Preeclampsia Scleroderma renal crisis Thrombotic Thrombocytopenic Purpura Mx bloods stool urinalysis haemolytic workup renal USS to rule out obstruction ?abx ?plasma exchange |
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Croup - laryngotrachebonchitis
(see rch) |
CROUP - parainfluenza/influenza/RSV.....
-barky seal cough, stridor, wheeze -worse at night, peak night 2-3 -fever but no signs of toxicity (uncommon <6month, rare <3months, alternate DDx) Mx -minimal examiniation -Ix not usually indicated MIld-mod: pred 1mg/kg and next night, d/c after 30mins if stridor free at rest Severe: neb adrenaline (5ml of adrenaline 1:1000.) AND Give 0.6mg/kg (max 12mg) IM/IV dexamethasone |
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preeclampsia
(see the womens guidline) |
MILD 140-149/90-99
MOD 150-159/100-109 SEVERE >160/110 (proteinuria, PCR >30) clonus, headache, visual disturbance, LFTs/epigastric, oedema (plts, uric acid) ?HELLP Blood: o group and hold o pre-eclampsia screen (FBE, U&E, Uric Acid, LFT’s o coagulation profile (APTT, PT, fibrinogen- if platelets <100x109 ) Mx IV labetolol or hydralazine fluid balance, IDC MG sulphate if severe indications as per guidlines |
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ectopic pregnancy Mx
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IF
-no significant pain -unruptured adenexal mass <35mm and no heart beat -hCG <1500IU/litre -no intrauterine pregancy can be offered methotrexate, can also be offered surgery Surgery is first line treatment if -significant pain -adenexal mass>35mm heart beat visible hCG >5000IU/L consider ANti D |
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dx acute appendictis
whos at most risk? mechanism? presetnation eamination signs? ddx? paediatrics |
70% age 10-30
lymphoid hyperplasia leads to luminal obstruction -often follows viral illness (as does medenteric adenitis) visceral pain begins ~17 HRS after obstruction average time to perforation = 34hrs presentation Seen in 60 %:Anorexia, Periumbilical pain, nausea, vomiting, RLQ pain developing over 24 hrs. Anorexia and pain are most frequent Usually nausea, sometimes vomiting Diarrhea, esp. with pelvic location Usually tender to palpation Rebound is a later finding Examination signs Tenderness at McBurney's point Cutaneous hyperesthesia in T 10 to 12 dermatomes Rovsing's sign (left palp=right pain) Psoas sign (passivbe hip ext, active hip flex) Obturator sign(external hip rotation) DDX in ovulating women -PID, ruptured cyst, torsion, ectopic, Endometriosis, Mittelschmertz (note appendix is most common surgical emergency inpregency) else: Gastroenteritis Mesenteric lymphadenitis Crohn's disease Diverticulitis UTI Pyelonepritis paeds Most common misdiagnosis is AGE Up to 50 % initially misdiagnosed < 2 yrs. : perforation rate approaches 100 % 3 to 5 yrs. = 71 % 6 to 10 yrs. = 40 % Sequence of pain and vomiting may be helpful Localized tenderness not a feature of AGE AND > age 60 : only 5 to 10 % diagnosed without delay Only 20 % classic presentation |
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Aspirated and Ingested Foreign Bodies
note 80% are pediatric 80% of adult oesophageal impactions have underlying oesophageal dz <10% ofpaeds have underlying dz 10-12% require endoscopy, 1% require surg (kids) effects /signs ddx of partial airway obstruction in children fishbone in oesophagus? oesophageal fb sx, mx indications for emergency removal xray signs of possible oesophageal perforation indications to admit a pt ingested a fb nasal fbs ear fbs rectal FB |
complete upperairway obstruction = death
partial upperairway = wheeze, chest pain, mucosal injury/bleeding lower airway obstruction = atelectesis, pneumonia, decr bs cxr findings - fb radio opaque 6-20% normal -= 18-33% else -obstructive emphysema -atelectasis -pneumonia (expiratory film enhances yield) ddx FB infections - croup, epliglottitis, abcess, diptheria neoplasms -haemangiomas, angiofibromas..... iatrogenic - leryngeal nerve paralysis, trancheal ulceration/granuloma, vocal cord granuloma other - lingual thyroid, allergic oedema, congential craniofacial anomolies fishbone in oesophagus? -only 20-35% with dysphagia after eating fish have fishbone -most are in posterior pharynx and retrivalble with magill forceps -for persistant symptoms endoscopy is needed (only 33-50% of fishbones show up on xray) note calcified arytenoid cartilages can mimc fish bone) sx -stridor, choking, gaggin, coughin, drooling, refusal to eat, spitting, vomiting, chest or neck pain (the person can often point to the level of obstruction , dysphagia mx xray x2 views ?glucagon.... endoscopy -follow up barium swallow in adults emergency removal if -sharp/-bone fragment -battery/corrosive -any sign of perforation xray signs oesophageal perf -air in : cervical soft tissue, subcutaneous, supraclavicular, mediastinum -pneumothorax -pleural effusion -retropharyngeal swelling ?admission -90% of ingested FB will pass in 7 days -admit if high risk object eg sharp points, cocaine packets, >6,5cm, potential toxin -multiple objects ->2weeks -signs of obstruction/abdominal pain/peritonitis, GIT bleeding EAR FB RECTAL FB -pevlic/abdo xray first -emergent surgery if any sign of perforation |
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Selected E.N.T. Emergencies Related to Sepsis
LIST sinutsitis Cx?: signs Ix Mx acute mastoiditis: usual bug, signs Mx, cx acute chondtritis - usual cause mucormycosis - fungal, immunocomprmised, mortality 30-70% peritonsilar abcess -signs, mx retropharyngeal, parapharyngeal abcess - signs, XRAY, mx ludwigs angina-what is it, big cx, mx vincents angina- what is it, acute epiglottitis -who most common in now?, SX? XRAY? MX? |
sinutsitis Cx?: abscess (frontal & orbital)
signs: periorbital/frontal cheekoedema proptosis, ophthalmoplegia, ptosis, diplopia meningeal signs neuro deficits cn ii - Vi need face ct for dx iv abx, admission, surgical drainage ACUTE MASTOIDITIS usually strep pneumonia signs: Most patients (>80%) have no history of recurrent otitis media. Persistent otorrhea beyond 3 weeks is the most consistent sign that a process involving the mastoid has evolved. Pain is localized deep in or behind the ear and is typically worse at night. Persistence of pain is a warning sign of mastoid disease. Mx: IV ABx, myringotomy & drainage mastoidectomy for resistant or complex cases be wary of necrotising external oitis/"malignant external otitis" (usually pseudomonas) acute chondtritis - usual cause - ear piercing peritonsilar abcess -uni lateral paritonsilar and soft palate swelling with uvular deviation -trismus, drooling, muffle "hot potoato" voice may need ct to rule out para pharyngeal abcess IV abx, neddle aspirtation +/- later tonsillectomy retropharyngeal, parapharyngeal abcess signs -neck swelling, muffled voice, fever, dysphagia, neck hyperextension XRAY distance from the anterior surface of the vertebrae to the posterior border of the airway: C2, 7 mm or less, regardless of the patient's age. C6/7, 14 mm or less in children < 15 years. 22 mm in adults [A simpler (but less precise) rule is that the soft tissue plain should be less than one half the width of the corresponding vertebral body.] Mx -CT to deliniate extent -IV abx, drainage, +/- intubation for airway protection Ludwigs angina -the most common neck space infection -rapidly swelling cellultitis +/- abcess, of the sublingual and submaxillary spaces -usually from tooth infections, usually poly microbial -most pts are toxic, severely ill, dehydrated -big cx = airway obstruction due to upward tongue swelling Mx - CT to deliniate any abcess, ?tracheostomy, IV abx, I&D, excision of source teeth vincents angina -acute necrotising infection of the pharynx and/or tonsils -fever, lymphadenopathy, metallic taste -need CT to look for gas in soft tissue +/-abcess -IV penicillin/clinadmycin, surgical debridement of necrotic tissue. acute epiglotitis - now most common in men 40-6- -febrile, toxic, drooling -thumbprint sign on xray -need ct to R/O abcess -mx IV ceftriaxone +/_ airway control (neb adrenaline) |
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Acute Sinusitis Diagnosis, Management, and Complications
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Oncologic Emergencies
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Emergency Department Management of the Abused Child
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Diagnosis of Dyspnea
DDX in order... |
big DDX to rule out fast
-anaphylaxis -ptx -FB/obstruction (food, tumour, abcess, infection, blood) -pe -asthma/bronchospasm -apo -tamponade -pneumonia -acidosis/DKA -flail chest -diaphragm/spinal cord injury -effusion-lung or cardiac -copd -dysrhytmia -anaemia causes of air hunger -mechanical -meetabolic -cerebral -psych |
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Crush Injury and Crush Syndrome
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Dog Attack! Dog Bite Injuries
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managing the violent patient
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-search for weapons
-chemical options **haloperidol 10mg IM, ?rpt 10-20mins if dystonic reaction need anticholinergic eg (benztropine 1-2mg im/iv or diphenhydramine) ** midazolam 2mg IM |
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nasal foreign bodies
sx cx exam techniques 2. |
NASAL FBs
may present as -unilateral rhonorrhoea, epistaxis, sinusitis Cx -bleeding is the most common cx -Local inflammation can result in pressure necrosis. ==> mucosal ulceration and erosion into blood vessels, ==> epistaxis. other Sinusitis (due to swelling and obstruction) Acute otitis media Nasal septal perforation Periorbital cellulitis Meningitis Acute epiglottitis Diphtheria Tetanus - adequate inspection of the nasal cavity, -assess for cx tympanic membranes?acute otitis media, ? sinusitis, ? nuchal rigidity in the toxic child, ?fb aspiration - auscultate the chest and neck for wheezing or stridor removal keep head stabilised - ?sedation, assistance equipment should include good light (head torch ) and airway equipment techniques -direct instrumentation: ideal for easily visualised, non spherical, non friable -balloon catheters: ideal for small round objects balloon is inspected,catheter is coated with 2% lidocaine jelly. With the pt supine, it is inserted past the FB and inflated with air or water (2mL in small children and 3mL in larger children). After inflation, the catheter is withdrawn, pulling the FB with it. -positive pressure: large occlusive FB 1, occluding the unaffected nostril and asking the child to blow hard out of his or her nose 2. "parents kiss" a tight seal is formed around the child's mouth, while avoiding the nose. The unaffected nostril is then occluded, and a forceful puff of air is provided (can use bage valve mask too but the Sellick maneuver should be applied to prevent esophageal air insufflation) -Suction : ideal for easily visualized, smooth or spherical foreign bodies. |
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ear foreign bodies
contraindications to removal? anaesthesia? position? technique? |
Contraindications
-perforation -incomplete visualisation of auditory canal -batteries (never irrigate!) local anaesthersia not usuallyneeded procedural sedation is sometimes needed position seated or lateral lying techniques mechanical extraction, irrigation, suction -irrigation contraindicated in organic material that may swell -live insects should be immobilised before removal eg oil or viscous lidocaine Abandon attempts to retrieve a foreign body if complications arise. -object migrates farther into the canal -bleeding, -edema, or - increasing pain develops, |
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ankle fractures
ring of bones &ligamnets? classification system? |
syndesmosis
delatoid ligament laterally anterior talo fibular ligament medially webber A,B,C type A -below level of the ankle joint -tibiofibular syndesmosis intact -deltoid ligament intact -medial malleolus often fractured usually stable : occasionally nonetheless requires an open reduction and internal fixation (ORIF) type B -at the level of the ankle joint, extending superiorly and laterally up the fibula -tibiofibular syndesmosis intact or only partially torn, but no widening of the distal tibiofibular articulation -medial malleolus may be fractured or deltoid ligament my be torn -variable stability type C -above the level of the ankle joint -tibiofibular syndesmosis disrupted with widening of the distal tibiofibular articulation -medial malleolus fracture or deltoid ligament injury present -unstable : requires ORIF |
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scaphoid fracture
boundaries of snuff box, & what runs through it> 3 parts of scaphoid?, blood supply? ?terry thomas sign mx indications for surgery |
bound by
extensor pollicis longus abductor pollicis longis * extensor pollicisbrevis radial styloid runs through -radial artery -cutanous sensation branch of radial nerve distal pole, waist, proximal pole radial artery supplies distal pole terry thomas sign = separation of lunate and scaphoid ~3-4mm, needs surgery if clinical indications but no fracture on xray should have rpt xray in 7-14 days ?fracture visible then Patients with non-diagnostic X-rays and a low clinical index of suspicion can be treated with a simple wrist splint with the decision on follow-up dependent on the patient, the doctor and their resources. Patients with a high index of suspicion or proven fracture with no indication for surgery should be immobilised. A Colles plaster has been shown to be at least as effective as a traditional short arm Scaphoid cast. The more proximal the fracture, the longer the healing time: Distal 1/3 - 6-8 weeks. Middle 1/3 – 8-12 weeks. Proximal 1/3 – 12-23 weeks. Indications for Surgery: -Displacement >1mm. -All proximal scaphoid fractures? (controversial) -All clearly visible fractues? (controversial) -Fractures associated with any degree of lunar tilt. -Non-union develops during follow-up. -Unwilling or unable to wear cast for 6-12 weeks. |
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colles fracture
*don't for get to look for avulsions as well what is it ? what bones transfer the energy to the radius? what other # occurs in 50% ligaments that can be damaged too? Cx? difference between smith and colles? Ix Tx report checklist |
extra-articular fractures of the distal radius
( fracture of the distal radial metaphyseal region with dorsal angulation and impaction, but without involvement of the articular surface.) scaphoid and lunate transfer energy both in dorsal direction and along the long axis of the radius 50% have ulnar styloid # palmar & dorsal radioulnar ligaments Cx -deformity/pain/dysfuntion -median nerve injury -extensor pollicis longus rupture (?ischaemic cause) smith # has volar angulation usually just plain xrays but if intraarticular concerns may need ct Tx -most just reduction and cast -cast in ulnar deviation & flexion -Open reduction and internal fixation should be considered when the fracture is unstable, and/or un-satisfactory closed reduction is achieved (e.g. >10 degrees dorsal angulation; >5mm shortening; significant comminution) Report checklist -fracture -degree of dorsal angulation -degree of impaction -degree and direction of displacement -location of the medial fracture line: does it involve the radioulnar joint -presence for intra-articular fractures other fractures -ulnar styloid -carpal bones |
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hand nerve examination
quick tests signs of palsy? |
note: there are no motor branches of the radial nerve in the hand
quick tests ulnar: abduct fingers & resist squeeze median: thumb to little finger and resist radial: wrist extension & resist ulnar nerve palsy = claw hand median = cannot ok radial - wrist drop (peroneal nerve = foot drop) |
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myotomes and dermatomes
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myotomes
c2: breathing C3-4: spontaneous breathing, trapezius fxn c4-6: shoulder flexion/extension C5: deltoid abduction at shoulder C6 biceps flexion at forearm, wrist extendion (ECR) C7: wrist flexion, elbow extension (tricveps) C8: middle finger flexion T1: little finger abduction/spread fingers L2-3: hip flexion (iliopsoas) L3-4: knee extension (quads) L4: ankle dorsiflexion (tib ant), foot inversion L5: big toe extension (EHL), foot dorsi flexion S1: ankle plantar flexion (calf), toe walking |
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retroorbital haematoma
-why is it bad? -presentation? -what to do? contraindications? |
acute orbital compartmewnt syndrome -Due to trauma, orbital plexus bleeds and results in ischemia of the optic nerve and retina
Pt presents withpain, decreased vision, diplopia, limited extraocular movements, proptosis, ecchymosis around the eye, bloody chemosis, increased intraocular pressure (IOP), resistance to retropulsion, and an afferent pupillary defect. leteral orbital canthotomy - lateral and medial canthal tendons attach the eyelids to the orbital rim and limit any anterior displacement of the globe -Without decompression, irreversible vision loss due to increasing orbital pressure may occur in as little as 90-120 minutes -contraindicated by suspected globe rupture eg hyphema; a peaked, teardrop-shaped, or otherwise irregularly shaped pupil; exposed uveal tissue, which appears reddish-brown; and extraocular movement restriction that is greatest in the direction of the rupture. method -local aneasthesia: Direct the needle tip toward the lateral orbital rim and begin injecting when the needle touches bone -consider restraining head/pt -1-2cm skin cut then find tendon and cut |
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shoulder dislocation
what is their analgesic position? |
abduction or adduction?
analgisc position adduction -humerus to full adduction -flex elbow -gentle continuous axial (down the length of the humerus) pressure abduction -(1) gently externally rotate the arm, and gently abduct the arm to between 30 and 100 degrees of abduction (2) provide gentle continuous axial (down the length of the humerus) pressure, (3) wait, and then ask if your patient is more comfortable. adduction use cunningham or kochers abduction use modified milch or scapular manipulation CUNNINGHAM This technique uses a combination of positioning and specific massage of the spasming biceps muscle. 1. positioning Face directly opposite to the patient and kneel next to them, their hand on your shoulder, operator’s wrist resting on the patient’s forearm 2. massage ask pt to shruf posteriorly, superiorly. massage biceps at mid humeral level, wait for pt to fully relax and humeral head slips back into place - tell pt not to fight the movement KOCHERS This technique externally rotates the humeral head, and then lifts it anteriorly past the glenoid rim back into place 1. positioning -sit up no slouching, against hard backed chair -arm id adducted next to body and elbow flexed to 90 2. slowly externally rotate until you feel resistance 3. lift/push the arm forwards/amteriorly keeping elbow at 90 4. finally internally rotate keeping elbow at 90 modified milch This technique uses a combination of scapular fixation and positioning the humerus in the Zero Position. It is useful for patients who are in abduction already, as is the Scapular Manipulation Method. 1. positioning Sit your patient in a hard backed chair and stand behind the affected limb. Place your left hand over the trapezius and spine of scapula. This fixes the scapula and informs you of any scapular movement during the procedure. Aim to get your patient comfortable by finding Analgesic Position 2. 2. Hold the right arm by the wrist. Slowly and gently abduct to 100°. Gradually externally rotate as the arm is lifted. 3. The humeral head may be gently pushed anteriorly (by your thumb or an assistant) if the relocation does not occur. SCAPULA manipulation technique This technique fixes the humeral head in position and then rotates the scapula around the head into position. 1. positioning The starting point for this is with the arm in 90° of forward flexion and externally rotated (providing the largest surface area of humeral head articular cartilage to the glenoid rim) NOTE This technique was originally described in 1979 (Bosley) with the patient prone, this is often impossible with elderly, obese or distressed patients. Two operators and a seated patient is probably the easiest option but prone (with weights giving traction) or supine are alternatives. 2. apply GENTLE traction Rest on the clavicle to steady the arm (and yourself). 3. After the patient begins to relax, rotate the scapula: Inferior tip – push medially Superior scapula – push laterally |
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abdominal pain
ddx |
GENERALISED ACUTE ABDO
perforated peptic ulcer perforation of other intrabdominal organs AAA rupture aortic dissection pancreatitis ectopic pregnancy ischemic gut CENTRAL PERICUMBILICAL acute small bowel ischemia acute appendicitis acute small bowel obstruction acute pancreatitis testicular torsion medical causes of abdominal pain EPIGASTRIC gastritis peptic ulcer reflux esophagitis pancreatitis cancer (gastric, pancreatic) Booerhaarve’s disease (esophageal rupture) dyspepsia irritable bowel syndrome Pain from nearby areas abdominal: central, RUQ pain cardiac: e.g. myocardial infarction, pleuritis pulmonary: e.g. pneumonia, pleurisy RUQ Gall bladder biliary colic cholecystitis cholangitis Liver hepatitis hepatomegaly (e.g. liver congestion in right heart failure) hemorrhage into hepatic tumour trauma hepatic or subdiaphragmatic abscess Fitz-Hugh-Curtis syndrome (periphepatitis due to PID) Other gastrointestinal appendicitis with high appendix (e.g. pregnancy) perforated or penetrating duodenal ulcer colon cancer Pain from nearby areas abdominal: epigastric, central, RIF, loin, groin pain right lower lobe pneumonia, pleurisy or other lung disease subphrenic abscess acute pyelonephritis LUQ pancreatitis subphrenic abscess diverticulitis ruptured spleen acute pyelonephritis leaking aneurysm of the splenic artery acute gastric distention RIF Gastrointestinal appendicitis crohns disease inflamed meckels diverticulum cholecystitis with low gall bladder mesenteric adenitis epiploic appendagitis colon cancer constipation irritable bowel syndrome Reproductive (female) ectopic pregnancy acute ovarian event (cyst rupture, hemorrhage, torsion) Mittelschmerz (ovulation pain mid-cycle) Pelvic inflammatory disease Endometriosis Reproductive (male) seminal vesiculitis undescended testicle pathology Urinary renal colic UTI Pain from nearby areas abdominal: RUQ, central, groin pain hip pathology psoas abscess rectus sheath hematoma right lower lobe pneumonia LIF Gastrointestinal diverticulitis colitis colon cancer constipation irritable bowel syndrome Reproductive (female) ectopic pregnancy acute ovarian event (cyst rupture, hemorrhage, torsion) Mittelschmerz (ovulation pain mid-cycle) Pelvic inflammatory disease Endometriosis Reproductive (male) seminal vesiculitis undescended testicle pathology Urinary renal colic UTI Pain from nearby areas abdominal: LUQ, central, groin pain hip pathology psoas abscess rectus sheath hematoma left lower lobe pneumonia SUPRAPUBIC urinary retention cystitis uterine in origin (e.g. PID, fibroid, menstruation) origin from RIF and/ or LIF causes LOIN PAIN Renal tract infection e.g. pyelonephritis obstruction, e.g. renal colic renal carcinoma renal vein thrombosis polycystic kidney disease adrenal hemorrhage Other retroperitoneal hemorrhage retroperitoneal infection vertebral pathology GROIN renal calculi scrotal pain e.g. testicular torsion, epididymorchitis, trauma inguinal hernia hip pathology pelvic fracture |
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endocrine emergencies
MOA -either deficit of hormine, excess of hormone or neoplasia MEN syndromes? poly endocrine failure syndromes? |
Adrenal
-Addisonian Crisis -Pheochromocytoma Thyroid -Thyroid Storm -Myxedema Coma Miscellaneous -Hypoglycemia -Diabetes Insipidus MEN I (Wermer) hyperparathyroid, pituitary adenoma, pancreatic ca MEN IIa (Sipple) hyperparathyroid, thyroid medullary CA, phaeochrom MEN IIb medullary thyroid Ca, phaeochromo, mucosal neuromas, marfinoid habitus POLY ENDOCRINE FAILURE SYNDROMES Type I Hypoparathyroidism Hypoadrenalism Mucocutaneous candidiasis Other (hypogonadism,autoimmune thyroid disease, JODM) Type II Adrenal insufficiency Autoimmune thyroid disease Other (JODM, primary or secondary gonadal failure) |
