medical and surgical emergencies and major trauma Flashcards
pre-hospital mx ACS
MONA:
morphine (IV 5-10mg with anti-emetics)
Oxygen (only if hypoxic)
Nitrates (sublingual IV, only if SBP>90mmHg)
Aspirin 300mg STAT (then 75mg OD thereafter)
mx acute STEMI
<12h Sx onset and PPCI within 120 minutes = PPCI
Otherwise,fibrinolysis
mx acute NSTEMI
Fondaparinux 2.5mg OD
DAPT = aspirin and ticagrelor
Coronary angiogram +/- stenting (speed of which depends on GRACE score)
secondary prevention ACS
5As:
Aspirin 75mg OD
Another antiplatelet e.g., clopidogrel 75mg OD/ticagrelor 90mg BD
ACEi e.g., ramipril
Atorvastatin 80mg ON
Atenolol (aka beta-blockers, usually bisoprolol)
Echocardiogram to assess systolic function
Cardiac rehabilitation
specific blood test if suspect MI
troponin
scoring system for mx MI
GRACE
moderate acute asthma
PEFR 50-75%
RR<25
HR<110
speech normal
severe acute astham
PEFR 33-50%
RR>25
HR>/= 110
unable to complete full sentences
life threatening acute asthma
PEFR<33%
Spo2<92%
silent chest and cyanosis
haemodynamically unstable
exaustion/altered GCS
ABG=normal co2
ix acute asthma exacerbation
Routine bloods e.g., FBC, U&E, LFTs, CRP,
Viral throat swabs
ABG
CXR
mx acute asthma exacerbation
O SHIT ME) -
Oxygen (>94%)
Salbutamol 2.5-5mg nebulised (oxygen driven)
Can trial IV if B2B nebs not helping
Hydrocortisone 100mg IV or PO pred 40-50mg
Ipratropium bromide 0.5mg nebulised QDS
Theophylline IV (senior staff/ICU decision)
Magnesium sulfate IV 2g (senior staff)
Escalate early – involve ICU if not improving
hyperkalaemia classification
Mild 5.5–5.9, moderate 6.0–6.4, severe ≥ 6.5
ECG features hyperkalaemia
Flattened P waves
Tall-tented T waves
Widened QRS
Sinusoidal pattern ventricular fibrillation
ix in hyperkalaemia
U+E
ECG
when to tx hyperkalaemia as an emergency
K+ ≥6.5 or ECG changes
mx hyperkalaemia
FIRST = calcium gluconate: Stabilises the myocardium, protects from VF
COMBINED insulin/dextrose infusion
Nebulised salbutamol
Calcium resonium
?Loop diuretics
Consider dialysis if refractory hyperkalaemia despite medical management
Suspend drugs that increase K+ e.g., ramipril, spironolactone etc.
A-E approach to tachycardia and bradycardia
O2 if <94%
IV access
monitor ECG, O2,
identify and tx reversible causes e.g. electrolyte abnormalities, hypovolaemia
life threatening features adult tachycardia/bradycardia
shock
syncope
myocardial ischaemia
severe HF
what to do if tachycardia with life threatening features
synchronised DC shock - up to 3 attempts
need sedation/anaesthesia if conscious
no success: amiodarone 300mg IV over 10-20mins
repeat shock
mx tachycardia with no life threatening features, broad and irregular QRS
consider:
-AF with bundle branch block -> control rate with BB, consider digoxin or amiodarone if HF, anticoag if duration over 48h
-polymorphic VT (torsades de pointes)-> magnesium 2g over 10 min
mx non life threatenin tachycardia with broad regular QRS
if VT or uncertain rhythm: amiodarone 300mg IV over 10-60min
if previous SVT with bundle branch block/aberant conduction: vagal manoevres, adenosine 6mg IV rapid bolus, then 12mg, then 18mg. verapamil or BB
if ineffective syncronised DC shock
mx non life threatening tachycardia with narrow regular QRS
- vagal manoevres
- adenosine 6mg IV rapid bolus, if ineffective 12mg, 18mg. need to monitor ECG
- if ineffective verapamil or BB
- syncronised DC shock
mx non life threatening tachcyardia with narrow irregular QRS
probable AF: rate control with BB, digoxin or amiodarone if HF, anticaog if duration over 48h
mx adult bradycardia with life threatening signs
atropine 500mcg IV
response and no risk asystole then observe
no response: interim measures = atropine 500mcg IV repeat to max 3mg, isoprenaline 5mcg/min IV, adrenaline 2-10 mcg/min IV
OR transcutaneous pacing
transvenous pacing
mx bradycardia with no life threatening signs and no risk asystole
observe
features in bradycardia at risk of asysteole
recent asystole
mobitz II block
complete heart block with broad QRS
ventricular pause >3s
most common causes pancreatitis
alcohol, gallstones and ERCP
presentation pancreatitis
Acute severe abdominal pain, vomiting, nausea, fever, tachycardia, shock, peritonitis.
ix pancreatitis
Obs, routine bloods, LFTs inc Amylase (or lipase), Calcium, ABG if requiring O2, USS/CT depending on clinical picture.
what is the imrie-glascow score
for pancreatitis
Reflects severity of inflammation alongside assess involvement/failure of other organs
factors in the imrie-glascow score
P–Pa02< 8 KPa
A–Age > 55
N–Neutrophils (WBC > 15)
C–Calcium < 2
R– uRea >16
E–Enzymes (LDH > 600 or AST/ALT >200)
A–Albumin < 32
S–Sugar (Glucose >10)
Interpretation of the imrie-glascow score
0-1 is mild, 2 is moderate and >3 is severe
atlanta classification pancreatitis
Mild: No organ failure or systemic complications
Moderate: Transient organ failure (<48 hrs) and /or local or systemic complications (sterile or infected) without organ failure
Severe: Persistent organ failure (>48 hours): single organ or multiple organ failure
mx pancreatitis
IV fluid resuscitation
Analgesia
Eat as able
Cholecystectomy ~ 6/52
CT if unwell 7-10 days after presentation
complications pancreatitis
NECROSIS IS BAD
Interstitial oedematous pancreatitis: Acute inflammation of pancreatic parenchyma and peripancreatic tissues, but without recognisable tissue necrosis
Necrotising pancreatitis: Pancreatic parenchymal necrosis or peripancreatic necrosis, or both
Acute peripancreatic fluid collection: Peripancreatic fluid with interstitial edematous pancreatitis but no necrosis (this term applies only within the first 4 weeks after onset of interstitial edematous pancreatitis and without features of a pseudocyst)
Pancreatic pseudocyst: Encapsulated collection of fluid with a well defined inflammatory wall usually outside pancreas with minimal or no necrosis (usually occurs > 4 weeks after onset of pancreatitis)
Acute necrotic collection: Fluid and necrosis associated with necrotising pancreatitis affecting pancreas or peripancreatic tissues, or both
Walled-off necrosis: Mature, encapsulated collection of pancreatic or peripancreatic necrosis with an inflammatory wall, or both (walled-off necrosis usually occurs >4 weeks after onset of necrotising pancreatitis)
cholelithiasis
Stones in gallbladder
features cholelithiasis
Asymptomatic (90%)
Biliary colic (10%)
mx cholelithiasis
USS to confirm gallstones, LFTs, add to (very long) elective list
cholecystitis
Inflammation of gallbladder
features cholecystitis
Pain – Murphy’s
Fever
N&V
mx cholecystitis
Confirm via USS - >4mm
10% may have obstructive jaundice picture
IVI + Abx – observe/operate
choledocholithiasis
Stone in CBD
presentation choledocholithiasis
Pain
Obstructive jaundice
mx choledocholithiasis
USS/MRCP
ERCP (usually pre-elective cholecystectomy)
cholangitis
Infection of the bile duct
presentation cholangitis
Pain
Fever/Septic
Obstructive jaundice
mx cholangitis
Septic screen and start IV Abx early. ERCP as above to treat the blockage.
pre-hepatic jaundice causes
haemolytic anaemia
gilberts
criggler-najjar syndrome
hepatocellular causes of jaundice
alcoholic liver disease
viral hepatitis
iatrogenic-medication
hereditary haemochromatosis
AI hepatitis
primary biliary cirrhosis or primary sclerosing cholangitis
hepatocellular carcinoma
post-hepatic causes of jaundice
intra-luminal e.g. gallstones
mural: cholangiocarcinoma, strictures,
extra-mural causes: pancreatic cancer
ALP
Biliary obstruction/stasis or bone turnover
ALT and AST
type of hepatic damage
albumin and clotting derangement
Liver damage ↓ synthetic ability
pre-hepatic jaundice bilirubin
cause a unconjugated hyperbilirubinemia – typically from excessive turnover of red blood cells that overwhelms the liver. This cannot be conjugated and secreted in the bile (and ultimately the urine/stool) so gets stuck on blood transport proteins and then skin/tissues.
hepatic jaundice bilirubin
Mixed jaundice of conjungated/unconjugated as cirrhosis can cause element of biliary obstruction (look at ALT/AST to work out)
post-hepatic jaundice bilirubin
Conjugated hyperbilirubinaemia
AST/ALT ratio
indicates the type of liver damage, if it’s 2 its liver damage, if roughly 1 its viral hepatitis, if it’s 0.4 it’s paracetamol
complications cholecystectomy
Gallbladder perforation is one – usually due to very inflamed/calcified gallbladder that is spiral down complications - wash out and IV Co-amox.
Bile duct injury - comes from difficult anatomy and being unable to identify calot’s triangle. Life changing injury.
duodenal ulcers
Pain when hungry eased by eating
gastric ulcers
Pain worse with eating
RF gastric and peptic ulcer
H Pylori associated with 95% of duodenal ulcers and 75% of gastric ulcers as causes increased acid secretion (increasing risk of ulceration). Also need to consider meds (NSAIDs, SSRIs, steroids, bisphosphonates). Rarely will be Zollinger-Ellison syndrome (gastrin producing tumour)
ix ulcers
FBC, Stool antigen/urea-13, OGD
mx gastric/duodenal ulcers
PPI and eradication therapy-lansoprazole + amox (metro if pen a) + clari/metro
features perforated peptic ulcer
sudden horrendous epigastric pain, looking shocked and likely peritonitis.
mx perforated peptic ulcer
Emergency – access, bloods (including ABG), erect CXR if cannot CT straight away (air-perforation). Give IVIs to maintain organ perfusion and get to theatre if unstable and evidence of unseal perforation. Lap or open, generally will need a washout
causes oesophageal bleed
Varices:
Oesophagitis:
Cancer:
Mallory-Weiss tear:
features oesophageal varices
bleed
Large volume, will likely be shocked and unstable. Will likely need intervention acutely to prevent re-bleeds
features oesophagitis
Usually small volume blood streaking vomit, preceded by GORD like symptoms
features oesophageal cancer
Will have s/s of Ca alongside a variable bleed. Can be small volume as tumour grows or a massive terminal event.
features mallory-weiss tear
bleed Will follow excessive vomit, usually self terminates
gastric causes GI bleed
ulcer
cancer
duodenal causes GI bleed
ulcer
what is blatchford score for
upper GI bleed
0=no intervention and discharge
>6 = urgent intervention
blatchford score
BUN
Hb: Men: 120-130 (1), 119-100 (2), <100 (6)
Women: 100-120 (1), <100 (6)
BP: 100-109 (1), 90-99 (2), <90 (3)
Pulse >100 (1)
Melaena (1)
Syncope (2)
Hepatic disease (2)
HF (2)
mx upper GI bleed
Resuscitate, 2x large bore cannulas, assess clotting. Assist clot formation if platelets under 50, fibrinogen is under 1 or PT/APTT is 1.5x normal with platelets/FFP
Endoscopy: Within 24 hours if severe bleed
If non-variceal: Endoscope and give PPI, if re-bleeds consider IR or laparotomy
If variceal: terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)
band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
rockall score use
post-bleed re-bleed risk, as rises so does re-bleeding risk (and then mortality risk)
features splenic rupture
blunt trauma
epigastric/LUQ pain with peritonism that gradually spreads as the spleen bleeds
ix splenic rupture
CT
mx splenic rupture
TLDR: If unstable – diagnostic laparotomy to assess damage
Conservative management: Small subcapsular haematoma, Minimal intra-abdominal blood, No hilar disruption (grade 3 and below). Resection if hilar injury/major haemorrhage.
If stable and grade 1-3 can closely observe and repeat CT in 1 week. Increasing tenderness has a low threshold to reimage +/- laparotomy. If contrast escapes during CT – use IR services to embolise vessel if available.
Critically: All patients who are treated conservatively should receive prophylactic vaccinations (against Strep Pneumoniae, Haemophilus Influenzae B (HIB) and Meningococcus) at discharge. If spleen comes out will need Pen-V for life as the spleen is so immunologically active in destroying Pneumococcus, Meningococcus, and H. Influenzae
grade 1 splenic injury
capsular tear <1cm parenchymal depth
subcapsular haematoma <10% SA
grade 2 splenic injury
capsular tear 1-3cm parenchymal depth
subcapsular haematoma 10-50% SA or intraparenchymal <5cm
grade 3 splenic injury
capsular tear >3cm parenchymal depth or trabecular vessels
subcapsular haematoma >50% SA or intraparenchymal >5cm
grade 4 splenic injury
laceration involving segmental or hilar vessels, devascualirsing >25% spleen
grade 5 splenic injur
completely shattered spleen or hilar vascular injury devascularising the entire spleen
presentation appendicitis
Young patient usually fit and well presents with single vomit, anorexia and generalised -> RIF pain.
Percussive and rebound tenderness -> peritonitis.
progression of generalised pain to McBurnies point,
ix appendicitis
80-90% will have neutrophil leucocytosis
Urine – rules out UTI/renal colic
USS: useful to rule out pelvic issues
mx appendicitis
Laparoscopic appendicectomy is gold-standard, if perforated will need copious washout. Conservative management with Abx works for most patients but a significant proportion will end up needing a lap appendix anway.
commonset causes small bowel bstruction
Adhesions (open > laproscopic)
Incarcerated hernia
Crohn’s
Malignancy
ix small bowel obstruction
CT
presentation small bowel obstruction
elderly with previous abdominal operations. They present, nauseous, vomiting +/- fecal, +/- distended, with episodic colicky peristaltic pain. Patient will have a period of BNO/no flatus being passed. Bowel sounds may appearing high pitched and ‘tinkling’ in early obstruction.
mx small bowel obstruction
NBM
Anti-sickness
IVI and hydrate
Decompress bowel with NG (gastrograffin)
If conservative management fails, surgery
Generally simple/partial obstructions are amenable to conservative management.
Closed loop obstructions tend to compromise arterial supply or venous return. Leading to bowel oedema and perforation/ischaemia/awfulness. Will likely require resection.
what is ileus
Deacceleration or arrest in intestinal motility – generally innocent
RF for ileus
Patient RFs: age, electrolytes, neurological disorders and anti-cholinergics
Surgical RFs: opioids, excessive handling of bowel, resection, contamination
ix ileus
Check electrolytes and inflammatory markers
mx ileus
innocent in the majority of patients, it can be a sign of otherintra-abdominal pathology
Manage with NG, fluids, daily bloods, encouraging mobilisation and reducing opioids
direct inguinal hernias
Bowel enters the inguinal canal “directly” through a weakness in the posterior wall of the canal, termed Hesselbach’s triangle
They occur more commonly in older patients, often secondary to abdominal wall laxity or a significant increase in intra-abdominal pressure
indirect inguinal hernia
Bowel enters the inguinal canal via the deep inguinal ring
They arise from incomplete closure of the processus vaginalis, an outpouching of peritoneum allowing for embryonic testicular descent, therefore are usually deemed congenital in origin
presentation inguinal hernia
lump in the groin, which (for reducible hernia) will initially disappear with minimal pressure or when the patient lies down. There may be mild to moderate discomfort, which can worsen with activity or standing. Check the cough impulse and try to reduce it yourself on examination.
mx inguinal hernias
Hernia repairs can be performed via open repair (Lichtenstein technique most commonly used) or laparoscopic repair.
femoral hernias
Entrance of abdominal contents into the femoral canal – much smaller with solid boundaries
presentation femoral hernias
elderly woman who has lost weight/fat which allows hernia through.
lump medial to femoral pulse
epigastric hernias
Abdominal contents breaches upper fibres of linae alba – low risk
spigelian hernias
Small tender mass at thelower lateral edgeof the rectus abdominus – high risk
presentation diverticular disease
Colicky, lower abdominal pain – relieved by defecation +/- altered bowel habit/flatulence/↕︎ bowel habit
presentation acute diverticulitis
Acute, tender, stabbing lower abdominal pain + s/s of systemic upset
classification diverticulitis
Complicated diverticulitis refers to abscess presence or free perforation
simple diverticulitis describes inflammation without these features.
RF for diverticulum
age, low dietary fibre intake, obesity, smoking, family history, and NSAID use.
mx diverticular disease
Patients with uncomplicated diverticular disease can often be managed as an outpatient* with simple analgesia and encouraging oral fluid intake. Outpatient colonoscopy should be arranged to exclude any masked malignancies.
mx diverticular bleed
conservatively as most cases will be self-limiting.
Those that fail to respond to conservative management may warrant embolisation or surgical resection. Indeed, if a second bleeding episode occurs there is a significant chance of further episodes (up to 50%)
mx acute diverticulitis
with antibiotics, intravenous fluids, and analgesia
mx perforated diverticulitis
Surgical intervention* is required in those with perforation with faecal peritonitis or overwhelming sepsis. This is a major procedure and usually involves a Hartmann’s procedure (a sigmoid colectomy with formation of an end colostomy. Fig. 3); an anastomosis with reversal of colostomy may be possible at a later date
AAA
Dilation of aorta >3cm – pulsatile mass o/e
mx AAA
3 – 4.5cm: yearly USS
4.5 – 5.4cm: 3m USS
>5.5cm/growing >1cm/yr/unstable – URGENT
presentation ruptured AAA
abdominal pain, back pain, syncope, or vomiting.On examination they will typically behaemodynamically compromised, with apulsatile abdominal massand tenderness.
mx ruptured AAA
Oxygen
Access
Urgent bloods including 6u crossmatched
Assess whether stable: If stable – CT angio to assess ?endovascular. If unstable get to vascular centre and laparotomy
cause renal/ureteric colic
calcium stones (oxalate > phosphate) but important rarer stones (e.g. struvite
narrowings in ureter
Pelviuteric junction
Pelvic brim
Vesicouteric junction
presentation ureteric/renal colic
Primary symptom is pain – colicky loin to groin +/- vomiting or tenderness in flank.
ix renal/ureteric colic
Check bloods and urine dip + CT KUB
mx renal/ureteric colci
Hydrate
PR Diclofenac +/- opiate +/- Abx
If obstructed/significant infection
Uteric stent
definitive: Extracorporeal Shock Wave Lithotripsy(ESWL, Percutaneous nephrolithotomy(PCNL, Flexible uretero-renoscopy(URS) and laser lithotripsy
common causes acute abdomen
ABDOMINAL: Appendicitis, Biliary tract, Diverticulitis, Ovarian, Malignancy, Intestinal (Obstruction), Nephritic, Acute pancreatitis, Liquor
AEIOUs: Acute (appendicitis/pancreatitis)/AAA, ectopic, IBD/intestinal, Obstruction/Ovarian, Uteric/Uterine, Stones
ix in acute abdomen
Urine, ABG, Routine Bloods, ECG and imaging
causes acute abdomen in R upper quadrant
cholecystitis
pyelonephritis
ureteric colic
hepatitis
pneumonia
causes acute abdomen in L upper quadrant
gasrtic ulcer
pyelonephritis
ureteric clic
pneumonia
causes acute abdomenin R lower quadrant
appendicits
ureteric colic
inguinal hernia
IBD
UTI
gynae/testicular torsion
causes acute abdomen in L lower quadrant
diverticulitis
ureteric colic
inguinal hernia
IBD
UTI
gynae/torsion
causes acute abdomenin epigastric region
peotic ulcer disease
cholecystitis
pancreatitis
MI
causes acute abdomen in peri-umbilical region
small and large bowel obstriction
appendicitis
AAA
radio opaque stones
Urate and xanthine
sepsis initial mx
Blood cultures
Urine output
Fluids
Abx
Lactate
Oxygen
RF sepsis
surgery, age, immunosuppression, diabetes, invasive lines, IVDU, open wounds
main classes of bacteria causing intra abdo sepsis
Gram –ve baccili e.g. e.coli,
Gram +ve cocci e.g. staph aureus
why is lactate measures in sepsis
Shows level of anaerobic respiration from hypoxic tissues
mx anaphylaxis
IM adrenaline 1:1000 500mcg (0.5mls)
IM/IV Chlorphenamine 10mg
IM/IV Hydrocortisone 200mg
common features analphylaxis
wheeze, urticarial rash, Tongue swelling, lip and mouth tingling, shortness of breath, fatigue, clammy, palpitations
Signs: tachypnoea, tachycardia, hypotension, drowsiness, wheeze, stridor
what causes hypotension in anaphylaxis
Histamine release causes mass vasodilation and capillary leak. This vasodilation reduces TPR and thus drops blood pressure. Capillary leak moves fluid from intra to extravascular space and thus drops total circulating volume.
CXR features in tension pneumothorax
Flattened R hemi-diaphragm, increased R intercostal spaces, total R sided collapse
Absent lung markings R side, mediastinal shift to L side, trachea deviated to L
mx tension pneumothorax
High flow O2 via 15L NRB, needle thoracostomy/chest drain insertion 2nd intercostal space mid-clavicular line
cautions following tension pneumothorax
Avoid flying for at least 1 month post pneumothorax. Do not fly until CXR proof that pneumothorax resolved. Never ever go scuba-diving
how to prevent tension pneumothorax recurring
Pleurodesis with sterile talc (either via chest drain or laparoscopic surgery), pleurectomy, or pleural abrasion (irritating pleura)
RF PE
Factors which cause hypercoagulability, venous blood stasis or vascular wall damage (Virchow’s triad)
score determining PE prognosis
PESI
interpreting wells score for PE
Score >4 : PE likely CTPA
Score <4: PE unlikely D-Dimer first CTPA if positive.
mx PE
anticoag- apixaban, rivaroxaban or LMWH
mechanism of action rivaroxaban
Factor Xa inhibitor
preventing PE
immediate mobilisation post surgery, TED stockings, LMWH prophylaxis
mx acute HF
: Furosemide and O2
daily wt and fluid balance chart
mx chronic HF
ACEI +BB
Spironolactone
Specialist stuff (hydralazine, nitrates, ivabradine, sacubitril valsartan)
CXR features HF
Alveolar oedema, kerley B lines, cardiomegaly, upper lobe diversion, pleural effusions
diagnosis HF
Transthoracic echocardiogram
to measure Left ventricular ejection fraction
mx bleeding varices
Stabilise patient with IVI, RBC, correct clotting abnormalities (platelets/FFB/Vit K)
Terlipressin 1-2mg every 4-6h until bleeding controlled
Antibiotics: broad spectrum abx cover e.g. IV co-amoxiclav 1.2g TDS
Urgent endoscopy for variceal banding or gastric sclerotherapy
TIPS (trans-jugular intrahepatic porto-systemic shunt) if varices resistant or recurrent.
severe hypovolaemia
Tachycardia >100bpm, hypotension <100mmhg systolic, CRT >3s, pallor, reduced GCS, urine output <0.5ml/kg/hr
lab ix after vomiting blood
FBC, U&E, LFTs, Crossmatch, clotting screen
mechanism causing bleeding oesophageal varices
Cirrhosis leads to portal hypertension (high pressure in portal venous system). When this pressure exceeds 10mmHg blood flow is redirected to a lower pressure system. This develops a collateral circulation around the lower oesophagus. As portal pressure increases, pressure increases in varices. They are thin walled and fragile and can burst causing UGIB.
diagnosing bleeding oesophageal varices
Upper GI endoscopy (OGD)
Glasgow Blatchford Score
can identify pts at low risk
(If GBS =0, risks of endoscopy outweigh benefits.)
Rockall Score
Calculates risk of re-bleeding and death
(good to know)
ix in MI
ECG, troponin at 0 and 3 h
later: CXR, echo
complications of MI
Arrhythmias (brady or tachy), Left ventricular failure, cardiac arrest, pericarditis/dresslers syndrome
RF MI
Smoking, Diabetes, hypertension, hypercholesterolemia, obesity, sedentary lifestyle, male gender, age, family history
medications discharged on after MI
B-Blocker, ACEI, aspirin, clopidogrel/ticagrelor 1 yr, Statin
driving after MI
4 weeks without driving if no successful revascularisation
1 week without driving if successful revascularisation
hyperkalaemia categories
Mild (5.5-6.5)
Moderate (6.5-8.0)
Severe (>8.0
when to tx hyperkalaemia
Treat hyperkalaemia if moderate/severe or if ECG changes
ECG changes mild hyperkalaemia
peaked T wave
prolonged PR
ECG changes moderate hyperkalaemia
loss of P wave
prolonged QRS
ST elevation
ectopic beats and escape rhythms
ECG changes in severe hyperkalaemia
widening QRS
sine wave
VF
asystole
axis deviation
bundle branch block
fascicular blocks
tx hyperkalaemia
Calcium Gluconate (10ml of 10% over 10min)
IV Insulin (10units) in IV glucose (50mls of 50%)
Regular monitoring of BMs and hourly K+ via bloods/VBG.
what can cause hyperkalaemia
medications: Spironolactone, lisinopril
AKI
reversible causes cardiac arrest
4H: hypoxia, hypovolaemia, hypo/hyperkalaemia, hypothermia
4T: thrombosis, tension pneumothorax, tamponade, toxins
shockable rhythms
VF/Pulseless VT
non shockable rhythms
Not shockable: PEA/Asystole
Which drugs are administered during a cardiac arrest?
Adrenaline 1mg IV/IO every 3-5mins,
Amiodarone 300mg IV/IO after 3 shocks
DKA definition
Hyperglycaemia ( >11.0mmol/L or known DM)
Acidosis (pH <7.3)
Ketonaemia ( >3.0mmol/L)
aims of DKA tx
Fall in ketones 0.5mmol/L/hr and glucose 3mmol/L/hr
Continue Insulin until ketones <0.3mmol/L, pH >7.3 and pt eating and drinking
mx DKA
IV 0.9% NaCl approx1L/hr
50units insulin in 50mls NaCl 0.9% at a rate of 0.1unit/kg/hr
Hourly VBG (glucose, HCO3- and K+) Add K+ to IVI as required
Add 10% glucose IV once BM <14mmol/l to run alongside NaCl
sx DKA
Drowsiness, vomiting, abdo pain, polyuria, polydipsia, lethargy, ketotic breath, deep breathing
non epileptic causes of zeizures
electrolyte abnormalities, alcohol withdrawal, benzodiazepine withdrawal, , hypoxia, hyponatremia, hypocalcaemia, hypoglycemia, uremia, encephalitis etc.
mx eplileptic seizures
Secure airway
High flow O2 and suction if required
IV lorazepam 4mg slow bolus if cannulated (buccal midazolam 5mg or rectal diazepam if not)
Repeat after 10 mins if seizure continues.
If seizures continue or recur in 30mins = Status Epilepticus
Phenytoin infusion 1-2g slow IVI (monitor BP and ECG)
ICU for RSI if lasting >60mins
initial approach
Control catastrophic haemorrhage
Airway and cspine
Breathin gwith ventilation
Circulation with haemorrhage control
Disability-neuro
Exposure/environment/everything else
MOI in major trauma
blunt force: RTC, assualt, fall
penetrating: shot, stab
sports
blast
how to handover
Age
Time
Mechanism
Injuries
Signs and obs
Treatment
mx catastrophic haemorrhage
direct pressire
indirect pressure: exclude proximal artery
torniquet: 2-3 inches above bleeding, 2nd one moreproximal if needed
haemostatic agents - ceetox
mx airway
jaw thrust
need to secure in 45m
rapid sequence indiction
c-spine
oxygen
listen and look
indications for intubation
cant mantain airway
cant oxygenate
cant mantain normocapnoea
decreasing consciousness
significant facial injury
seizures
burns: hypoxaemia, hypercanoea, deep facial, full thickness neck
relative: haemorrhage, shock, agitated, multiple painful injuries, transfer
canadian c spine high RF
> 65
MOI: fall >1.5m, axial load
paraesthesia
canadian spine low RF
minor rear end motorcollison
comfortable sittinhg
ambulatory
no midleine tenderness
delayed onset neck pain
when ti imobilise c spine
canadian c spine
any high RF
if low RF and cant rotate head 45 degrees L and R
life threatening thoracic injuries
airway obstruction
tension pneumothorax
open pneumothorax
massive haemorrhage
flail chest
cardiac tamponade
features tension pneumothorax
blunt or penetrating injury
tracheal deviation late sign
increased HR, decreased BP, hypoxia, agitated
massive haemothorax
> 15oo ml blood or >200ml/hr
presentation massove haemothroax
decreased air sounds
hyporesonant
mx open pneumothorax
3 sided seal dressing or will turn to tension pneumothorax
what is flail chest
fractured 2 or more ribs in 2 or more places
moves paradoxically during respiration
features cardiac tamponade
becks triad: decreased bp, decrased heart sounds, distended neck veins
mx cardiac tamponade
thoracotomy
signs of bleeding
decreased consciius, pale, sweaty, agitation, anxious
increased hr, increased rr, increased crt, narrow pulse pressure
bleeding compartments
thorax
abdo
pelvis
long bones
mx bleeding
permissive hypotension as too much fluid moves clot and makes worse
tranexamic acid
measuring neuro diability
AVPU
pupil size and response
GCS:motor best predictor
cushings triad
decreased HR and increased bp due to increased icp
irregular breathing
mx disability
prevent secondary brain injury
secure airway if gcs less than 8
control ventilation
normal icp, glucose and oxygen
what to look for in everything else
lumbs
keep warm
pain relief
what is major trauma
injury severity score (retrospective) >15
what is silver trauma
> 65s
most commonly fal from standing
why does silver trauma happen
osteoporosis
polypharmacy
blood thinners
decresaed muscle mass, balance, stiff joints
radiology in trauma
now use CT
mechanism anaphylaxis
type 1 hypersnesitivity rxn which causes mast cell degranulation and histamine release
mx anaphylaxis
remove stimulus
A-E: focus on airway and 2 large bore cannulae
IM 1:1000 adrenaline to thigh (0.1mg <6m, 0.15mg 6m-6y, 0.3mg 6-12y, 0.5mg adults)
observation post anaphylaxis
24-48 hrs as biphasic rxn - more common in children
ix once stable after anaphylaxis
serum mast cell tryptase
also another within 6h
options for getting blood
group and save: get NONE - learn type and save
cross match: takes 45m
type specific: 20m, rarely used
O negative: can get from A&E and theatres and give to anyone
major haemorrhage protocol: 2222 and say MHP=4 uits RBC, 1 platelets, 3FFP brought by porter
what do you get in the major haemorrhage protocol
4 units RBC
1 platelts
3 FFP
and a porter to bring it all
Raised pCO2 and normal pH on ABG mx
Compensated
Therefore no panic
Sats 88-92%
Repeat ABG IF O2 demand increases
Raised PCO2 AND low PH mx
Acute T2RF
Urgent senior rev
Sats 88-92%
NIV (BiPAP)
T2RF causes
Copd
Obstructive sleep apnoea
Motor neurone disease
Guillean barre
Myasthenia gravis
Scoliosis
Resp fatigue
Opiates
Sedatives
Naloxone dose
IV or IM if no access
Can bolus 400mcg but usually give in smaller increments (50) unless peri arrest
Approach to reduced urine output
Is it actually low: norm=0.5ml/kg/hr, is it being measured accurately
Why: pre-renal (fluid status, med rev, sepsis), renal (urine dip), post renal (retention-bladder scan)
Ix; U&E, VBG hly input output chart
Trial IV fluid or encourage to drink if compliant
First mx low urine output
CHECK CATHETER
flush
Check isn’t clamped
Mx hyperkalaemia
ALL AT THE SAME TIME
Cannula and repeat U&E
ask nurse to do ECG
Prescribe and ask nurses to givr calcium gluconate (1st priority) and insulin dextrose (50ml 50% Dextrose fluid with 10 units insulin in)
Senior input
Tx cause (AKI)
Other options for reducing K: salbutamol neb, sodium zirconium cyclosilicate/calcium resonium
Monitor response - need cardiac monitoring (if not on CCU/resus put on the defib Monitor), VBG within an hr
Monitor blood glucose
Less than what level is it unlikely to have ECG changes in hyperkalaemia
6
F1 role in major haemorrhage
FLUID BOLUS - ask nurse
2222 - major haemorrhage protocol +/- cardiac arrest
Bleep med reg
Try and limit bleeding - press artery, not much can do if GI
GET MORE ACCESS - large bore cannulas
Falls rev
Stable or caused by acute event (PE, bleed, stroke)
? CT head : anticoag, neurology, HI sx NICE CRITERIA
Other injuries: c spine, hips, joints
Why: Trip, BP, ECG
prevent: physio, mobility, supervision
