Acute Care and Trauma Flashcards
Define diabetic ketoacidosis
DKA is an acute metabolic complication of type 1 diabetes mellitus that is potentially fatal and requires prompt medical attention. It is characterised by absolute insulin deficiency.
What is the biochemical triad of diabetic ketoacidosis and describe the onset?
Hyperglycaemia
Ketonaemia
Acidaemia
There is RAPID onset.
Summarise the epidemiology of diabetic ketoacidosis?
In DKA, there is a reduction in the net effective concentration of circulating insulin and an elevation of counter-regulatory hormones (glucagon, catecholamines, cortisol, and growth hormone).
This leads to metabolic derangements and ketone production.
What are common precipitating events of DKA and risk factors?
Two most common precipitating factors:
Inadequate insulin therapy
Infection
Other risk factors: Underlying medical conditions eg MI or stroke - release of counter-regulatory hormones Drugs that affect carbohydrate metabolism (corticosteroids, thiazides, pentamidine, sympathomimetic agents, second-generation antipsychotic agents) SGLT-2 inhibitors Pancreatitis Acromegaly Hyperthyroidism Cushing's Syndrome
Summarise the epidemiology of DKA
Less common with increasing age
0-128 per 1000 people
What are the presenting symptoms of DKA?
Polyuria Polyphagia Polydipsia Weight loss Weakness Nausea and vomiting Abdominal pain Drowsiness Confusion Coma
What are the signs on physical examination of DKA?
Signs of dehydration - dry mucous membranes, poor skin turgor, sunken eyes
Tachycardia
Hypotension
Kussmal respiration - rapid and deep respiration due to acidosis
Acetone breath
Hypothermia
What are appropriate investigations for DKA?
Bloods: PLASMA GLUCOSE - high (>13.9mmol/L) Capillary or serum KETONES - BOHB >3.8mmol/L SERUM UREA - elevated due to volume depletion SERUM CREATININE - elevated Serum sodium - low Serum potassium - elevated FBC - elevated WCC
ABG - acidosis, low bicarbonate
URINALYSIS - positive for glucose and ketones, in presence of infection positive for leukocytes and nitrites
What is the management of DKA?
Intravenous fluids (0.9% saline)
Supportive care (ICU admission)
Potassium therapy if hypokalaemic (often caused by insulin therapy and correction of acidaemia)
IV dextrose when glucose reaches 15mmol/L
Intravenous insulin once serum potassium normalises
Add vasopressors, bicarbonate therapy and phosphate therapy
Monitor blood glucose, ketones, urine output and VBG
What are the possible complications of DKA?
Hypoglycaemia if excessive insulin therapy
Hypokalaemia due to bicarbonate and insulin therapy
Thromboembolic events - give heparin prophylaxis
Non-anion gap hypercholaraemic acidosis – due to urinary loss of ketoanions
Cerebral oedema
Acute Respiratory Distress Syndrome
What is the prognosis of DKA?
Mortality rate of 5%
Prognosis worse at age extremes or in presence of coma or hypotension
Define anaphylaxis
A severe hypersensitivity reaction characterised by rapidly developing life-threatening breathing or circulation problems and an associated urticarial skin rash.
Summarise the aetiology of anaphylaxis
Hypersensitivity of the immune system to a non-harmful antigen resulting in mast cell and basophil degranulation
Histamine causes bronchi and GI smooth muscle constriction and blood vessel dilation and permeability
Mainly IgE antibody mediated
In rare cases, immune complex mediated (opioids, contrast medium)
Can be non-immunologic
Causes: Food allergy - shellfish, peanuts, eggs Bee sting Drugs - antibiotics eg penicillin, NSAIDs Latex
Summarise the epidemiology of anaphylaxis
Food allergy anaphlyaxis most common in young children
Food allergy affects both sexes equally
Medication most common cause in adults
What are the presenting symptoms of anaphylaxis?
Angioedema - swelling of face, eyes, mouth Utricarial rash - red, itchy, blotchy rash with central white papule Shortness of breath Cough Wheeze Abdominal cramping Vomiting Diarrhoea Pruritis
What are the signs on physical examination of anaphylaxis?
Hypotension Tachycardia Use of accessory muscles Wheeze Stridor and hoarse voice Chest hyperinflation Cyanosis Pale clammy skin
What are the appropriate investigations for anaphylaxis?
Mainly a clinical diagnosis
Serum tryptase, histamine and IgE will be raised
ABG - metabolic acidosis
What is the management of anaphylaxis?
ABCDE assessment
IM ADRENALINE
Airway support and supplemental O2
IV fluids
Antihistamine
Corticosteroids to reduce chance of biphasic reaction
Allergy testing to prevent further reactions
What are the possible complications of anaphylaxis?
MI Loss of consciousness Respiratory arrest Death Recurrence
What is the prognosis of anaphylaxis?
Individuals with previous reactions puts them at increase risk of recurrence
Define acute kidney injury
An acute decrease in kidney function, leading to an increase in creatinine and a decrease in urine outflow. This results in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes.
Rise in serum creatinine of > 26micromol/L within 48 hours
Rise in serum creatinine of > 1.5 times the baseline over 7 days
Urine output <0.5ml/kg/hr for > 6 hours
Summarise the aetiology of acute kidney injury
Pre-renal:
Decreased renal perfusion - dehydration, third spacing due to sepsis or acute appendicitis, renal artery stenosis, heart failure
Hypovolaemia - acute haemorrhage, severe vomiting or diarrhoea)
Cirrhosis
Nephrotic syndrome
Hypotension - shock, sepsis, anaphylaxis
Medications - NSAIDs, ACE inhibitors, ARBs
Hepatorenal syndrome (hypoalbuminaemia due to decompensated liver failure)
Intrinsic renal:
Glomerulonephritis - nephritic or nephrotic syndrome
Nephrotoxin exposure - antibiotics, methotrexate, heavy metals
Acute interstitial nephritis (autoimmune, NSAIDs)
Glomerular: glomerulonephritis, haemolytic uremic syndrome
Tubular: acute tubular necrosis (secondary to ischaemia)
Vasculitides (e.g. Wegener’s granulomatosis)
Eclampsia
Post-renal (due to obstruction): Urinary calculi Prostatic cancer BPH Abdominal tumour eg bladder Urethral stricture
Summarise the epidemiology of acute kidney injury
Pre-renal acute kidney injury is the most common
It is most commonly seen in adults
15% of adults admitted to hospital will develop an AKI
What are the presenting symptoms of acute kidney injury?
Depends on the underlying cause ie if urinary calculi, will have renal colic
Anuria/oligouria
ABRUPT ANURIA SUGGESTS POST-RENAL OBSTRUCTION
Confusion
Nausea/vomiting
Dehydration
What are the signs on physical examination of acute kidney injury?
Hypotension
Signs of dehydration: Dry mucous membranes, postural hypotension
Tachycardia
Distended bladder if due to post-renal obstruction
Fluid overload (HF, cirrhosis, nephrotic): raised JVP, pulmonary/peripheral oedema
Pallor, rash, bruising (vascular disease)
What are the appropriate investigations for acute kidney injury?
Depends on cause
Bloods: FBC - anaemia, leukocytosis, thrombocytopenia U&Es - check for hyperkalaemia Blood culture if suspecting sepsis Creatinine - measure eGFR - high PSA - elevated if BPH, prostatic cancer ABG - metabolic acidosis
Abdo USS if suspect obstruction
CXR - pulmonary oedema
AXR - renal stones
Urinalysis - urine dip and microscopy:
Blood - nephritic cause
Leucocyte esterase and nitrites - UTI
Glucose, protein and urine osmolality
Immunology:
Serum immunoglobulins and protein electrophoresis: for multiple myeloma and Bence-Jones proteins in the urine
ANA and anti-dsDNA: associated with SLE
Complement levels: low in active lupus
Anti-GBM antibodies: Goodpasture’s syndrome
Antistreptolysin-O antibodies: high after Streptococcal infection
Virology: check for hepatitis and HIV
What is the management of acute kidney injury?
- Avoid nephrotoxic agents
- Remove drugs such as antibiotics, NSAIDs, ACEi
- No radiocontrast procedures - Manage fluid levels
- If signs of dehydration - IV fluids eg saline, vasopressors eg noradrenaline
- If signs of fluid overload - fluid restriction, furosemide - Protect from hyperkalaemia
- Give IV calcium gluconate - protect heart
- Give IV insulin and glucose - Dialysis if AKI refractory to treatment
Indications: Refractory hyperkalaemia, Refractory pulmonary oedema, metabolic acidosis, uraemic complications eg pericarditis, uraemic encephalopathy
Monitor serum creatinine, sodium, potassium, calcium, phosphate and glucose
Identify and treat infection
Urgent relief of urinary tract obstruction
Refer to nephrology if intrinsic renal disease is suspected
What are the possible complications of acute kidney injury?
Metabolic acidosis Hyperkalaemia Uraemic complications - pericarditis, uraemic encephalopathy Fluid overload CKD End stage renal disease Pulmonary oedema
What is the prognosis of acute kidney injury?
Inpatient mortality varies depending on cause and comorbidities
Indicators of poor prognosis: Age, multiple organ failure, oliguria, hypotension, CKD
Patients who develop AKI are at increased risk of developing CKD
Irreversible in 5-7% of adults
Define burns
Burns are very common injuries, predominantly to the skin and superficial tissues, caused by heat from hot liquids, flame, or contact with heated objects, electrical current, or chemical.
Severity is assessed by burn size (% total body surface area) and depth (first to fourth degree).
Summarise the aetiology of burns
Thermal burns: heat from hot liquids, flame, or contact with heated objects
Young children - 70% of burns caused by scalding from hot liquids
Older children and young working adults, flame injuries are more likely
Older adults, scalds and cooking accidents are most common
Electrical burns
Chemical burns: exposure to industrial or household chemical products
Non-accidental burns: Approximately 20% of burns in younger children involve abuse or neglect
Radiation burns
Summarise the epidemiology of burns
Difficult to determine as many people do not seek medical help
250,000 people suffer burn injuries in the UK
What are the presenting symptoms and signs on physical examination of burn injuries?
1st degree burns - dry, red, painful, blanching skin affected
2nd degree - red, clear blisters, wet, weepy, blanching, painful
2nd degree deep partial thickness - colour variation (white, red, yellow), blisters, may not blanch
3rd degree - dry, waxy white, leathery grey, no blanching, stiff, inelastic, pain due to deep pressure
4th degree - charred black, dry, patches of dead skin
Blistering sloughing skin
Underlying wet, tender erythema
Flame injury can present with leathery burns
What are the appropriate investigations of burn injuries?
Mainly clinical diagnosis FBC: Low haematocrit Hypovolaemia Neutropenia Thrombocytopenia
Metabolic panel:
High urea, creatinine, glucose
Hyponatraemia
Hypokalaemia
Carboxyhaemoglobin high if inhalational injury
ABG - metabolic acidosis if inhalational injury
Wound biopsy and histology if suggestions of infection
Define aspirin overdose
Excessive ingestion of aspirin causing toxicity
> 150mg/kg/day
Severity is dose-dependent >150mg/kg: mild >250mg/kg: moderate >500mg/kg: severe >700mg/kg: potentially fatal
Summarise the aetiology of aspirin overdose
Accidental ingestion
Self-harm
Attempted suicide
Incorrect dosage in children or older adults
Salicylate activates respiratory centre - causes respiratory alkalosis
Compensatory urinary excretion of bicarbonate and potassium - METABOLIC ACIDOSIS
Summarise the epidemiology of aspirin overdose
One of the most common drug overdoses
Accidental overdose in children and overdose for attempted suicide decreased following introduction of maximum number of aspirin you could purchase
What are the presenting symptoms of aspirin overdose?
Initially asymptomatic Fever, sweating, flushing Nausea, vomiting, dehydration, epigastric pain Tinnitus, deafness, vertigo Shortness of breath
Late stages: Lethargy Confusion Convulsions Coma Respiratory distress Drowsiness
Rare: non-cardiogenic pulmonary oedema
What are the signs on physical examination of aspirin overdose?
Tachypnoea
Tachycardia
Fever
Epigastric tenderness
What are the appropriate investigations of aspirin overdose?
Serum salicylates - elevated
Serum ketones - elevated
ABG - respiratory alkalosis followed by metabolic acidosis
Electrolytes - hypokalaemia, hypocalcaemia, hypomagnesaemia
LFTs - elevated AST and ALT if hepatotoxicity
Clotting - elevated PT
Toxicology
CXR - pulmonary oedema
ECG - hypokalaemia - small T waves, U waves
Define opiate overdose
Ingestion of a larger quantity of opioids that can be physically tolerated, resulting in dangerous CNS and respiratory depression, miosis and apnoea
Summarise the aetiology of opioid overdose
Substance abuse in regular users of illict or prescription opioids
Unintentional overdose for pain relief
Intentional overdose - self-harm, suicide
Iatrogenic
Recent abstinence in chronic users leading to decreased tolerance
Increased toxicity at lower dose due to: Hypothyroidism Hypotension Asthma Renal or hepatic impairment
Risk Factors: Mental health conditions Alcoholics Opioid abuse and dependence Recent abstinence in chronic users Morphine toxicity at a lower dose
Summarise the epidemiology of opioid overdose
The elderly are at greater risk because they are more likely to be on opiates
Heroin and morphine are responsible for most drug-related deaths
Most common cause of death of former inmates after leaving prison due to loss of tolerance
What are the presenting symptoms of opioid overdose?
Constipation (decreased GI motility if chronic) Altered mental status Coma Pink frothy sputum if causes ARDS Seizures Nausea and vomiting Loss of appetite Sedation Craving the next dose Drowsiness (if acute overdose)
What are the signs on physical examination of opioid overdose?
Miosis/pinpoint pupils Bradypnoea (reduced RR) Needle or track marks Pulmonary rales if causes ARDS Respiratory depression Hypotension and tachycardia
What are the appropriate investigations of opioid overdose?
Toxicology screen
Therapeutic trial with IV naloxone (opioid antagonist) - shows reversal of overdose symptoms
ECG - check for myocardial ischaemia
CXR - may show ARDS
Define paracetamol overdose
Excessive ingestion of paracetamol causing toxicity
Acute overdose is ingestion >4g or >75mg/kg in <1 hour
Summarise the aetiology of paracetamol overdose
Intentional overdose - self-harm or suicide
Therapeutic error - consistently taking small amounts over appropriate dosage
Incorrect dosing
The maximum recommended dose is 2 x 500 mg tablets (allows 4 times in 24 hours)
Intake > 12 g can cause hepatic necrosis
Risk Factors: Chronic alcohol abusers History of self-harm History of frequent or repeated use of medications for pain relief Patients on enzyme-inducing drugs (e.g. anticonvulsants) Malnourished Anorexia nervosa Pre-existing liver disease Acute or chronic starvation
Summarise the epidemiology of paracetamol overdose
Paracetamol is the most common drug used in overdose in the UK - 48% of poisoning admissions to hospital
Causes 100 deaths per year in the UK
What are the presenting symptoms of paracetamol overdose?
First 24 hours:
Asymptomatic
Mild GI disturbance - nausea, vomiting, anorexia, abdominal pain, lethargy, malaise
24-72 hours:
RUQ pain
Vomiting
72+ hours: Increased confusion (encephalopathy) Jaundice Decreased consciousness level Asterixis
What are the signs on physical examination of paracetamol overdose?
Less than 24 hours: no signs
24-72 hours: hepatomegaly, RUQ tenderness
72+ hours: jaundice, coagulopathy, hypoglycaemia, renal angle tenderness, asterixis
What are the appropriate investigations for paracetamol overdose?
Serum paracetamol - peak levels 4hrs after ingestion
AST and ALT - elevated
Arterial pH and lactate - acidaemia and elevated lactate
U+Es - renal impairment
PT - prolonged
INR - increased
Define thalassaemia
An autosomal recessive disorder caused by defective globin chain synthesis, due to reduced or absent alpha or beta chains.
Summarise the aetiology of thalassemia
Alpha:
Autosomal recessive mutation in one of the 4 alpha genes on chromosome 16
1 abnormal gene = asymptomatic silent carrier
2 abnormal genes = alpha thalassemia minor, mild microcytic anaemia
3 abnormal genes = HbH disease/alpha thalassemia major, microcytic anaemia and hepatosplenomegaly
4 abnormal genes = Hb Bart’s hydrops fetalis - incompatible with life
Beta:
Autosomal recessive mutation in one of the beta genes on chromosome 11
1 gene with reduced or absent synthesis - beta thalassemia minor
2 genes with reduced synthesis = beta thalassemia intermedia
2 genes with absent synthesis = beta thalassemia major
Summarise the epidemiology of thalassemia
More common in Africa, Mediterranean and South-East Asia
What are the presenting symptoms of thalassemia?
Alpha thalassemia minor and HbH disease:
Pallor
Shortness of breath
Fatigue
Beta thalassemia major: Pallor Shortness of breath Fatigue Jaundice Ascites Growth retardation Symptoms of haemochromatosis Failure to thrive Prone to infection
Alpha and beta trait:
May be asymptomatic
Detected in routine bloods or due to family history
What are the signs on physical examination of thalassemia?
Beta thalassemia major: Ascites Hepatosplenomegaly Jaundice Enlarged head and cheeks - chipmunk facies Pallor Frontal bossing
What are the appropriate investigations for thalassemia?
FBC - microcytic anaemia, decreased MCH
Peripheral blood smear: microcytic hypochromic RBCs, target cells, golf ball-like cells in alpha thalassemia, high reticulocyte count
Hb electrophoresis:
Alpha - HbH band in HbH disease
Beta - decreased HbA, increased HbF and HbA2
Genetic testing
Beta thalassemia major: Unconjugated bilirubin - elevated LDH - elevated Serum iron, ferritin and transferrin - increased Abdo USS - hepatosplenomegaly Skull X-Ray - hair on end sign
Bone Marrow biopsy - Hypercellular, erythroid hyperplasia
