Emergency Conditions Flashcards

Question

How is haemorrhagic shock classified

Answer 1

Type I -Volume of blood loss (ml): <750 -Percentage blood loss (%): <15 -Heart rate (beats/min): <100 -Blood pressure: normal -Pulse pressure: normal/increased -Respiratory rate (breaths/min): 14-20 -Urine output (ml/hour): >30 -Mental state: slightly anxious Type II -Volume of blood loss (ml): 750-1500 -Percentage blood loss (%): 15-30 -Heart rate (beats/min): 100-120 -Blood pressure: normal -Pulse pressure: decreased -Respiratory rate (breaths/min): 20-30 -Urine output (ml/hour): 20-30 -Mental state: mildly anxious Type III -Volume of blood loss (ml): 1500-2000 -Percentage blood loss (%): 30-40 -Heart rate (beats/min): 120-140 -Blood pressure: decreased -Pulse pressure: decreased -Respiratory rate (breaths/min): 30-40 -Urine output (ml/hour): 5-15 -Mental state: anxious, confused Type IV -Volume of blood loss (ml): >2000 -Percentage blood loss (%): >40 -Heart rate (beats/min): >140 -Blood pressure: decreased -Pulse pressure: decreased -Respiratory rate (breaths/min): >35 -Urine output (ml/hour): negligible -Mental state: confused, lethargic

Answer 2

Initial: ABCDE assessment Airway management High flow 02 non-rebreathe to >94% sats Obs monitoring Three lead cardiac monitoring ECG request Portable CXR Large bore IV access and take bloods and blood gas Fluid resuscitation IV Catheterisation and fluid balance monitoring (aiming output >0.5ml/kg/hr) If BP fails to respond, refer to HDU/ICU for: - central line insertion with central venous pressure and central venous oxygen saturation monitoring - arterial line insertion and invasive arterial BP monitoring - vasopressor and/or inotrope infusion Further: Identify and treat the cause: -Haemorrhagic -- identify bleed and acheive control -- restoration of adequate circulating volume --- crossmatch blood and activate major haemorrhagic protocol --- transfuse o neg until cross matched blood available (ASAP) -- Correct coagulopathy by transfusion of platelets, fresh frozen plasma and cryoprecipitate as appropriate -Septic -- antibiotics -- source control -Anaphylactic -- adrenalin 0.5mg IM -Tension pneumothorax -- needle thoracentesis -- intercostal chest drain insertion -Cardiac tamponade -- Pericardiocentesis -- Thoracotomy -Massive PE -- Thrombolysis -Unstable tachyarrhythmias -- Synchronised direct current cardio version -Unstable bradyarrhythmias -- Pacing

Answer 3

Usually immediately after an accidental ingestion or inhalation of known drug or chemical but may present later in intential overdose Acute confusional states Hypoglycaemia Abnormal liver function tests Unexplained seizures Abnormal bleeding Several close contacts presenting with similar symptoms such as headache and confusion - ?CO poisoning in house Recurrent or chronic unexplained symptoms in children (deliberate poisoning in Munchausen by proxy or factitious disorder)

Answer 4

Frequently asymptomatic Symptoms: Nausea and vomitting Anorexia Malaise Abdominal pain Altered mental status Confusion Evidence of previous self harm eg scars Signs: Asterixis Bruising Jaundice Right upper quadrant pain Oliguria/ anuria Tachycardia/ hypotension Coma

Answer 5

3-4 days after overdose and may lead to liver failure, hypoglycaemia, encephalopathy, coma and death

Answer 6

Hyperventilation Tinnitus Deafness Vasodilation Sweating Coma in severe poisoning

Answer 7

Dry mouth Seizures Coma Cardiac conduction defects and Arrhythmias Hypothermia Hypotension Hyperreflexia Extensor plantar response Convilsions Respiratory failure Dilated pupils Urinary retention

Answer 8

Nausea Vomiting Agitation Tremor Nystagmus Drowsiness Sinus tachycardia Convulsions Hyperthermia Rhabdomyolysis Renal failure Coagulation deficiencies Rarely can result in serotonin syndrome with marked neuropsychiatric effects, autonomic instability and neuromuscular hyperactivity

Answer 9

Bradycardia Hypotension Syncope Conduction abnormalities Heart failure Drowsiness Confusion Convulsions Hallucinations Coma (in severe cases)

Answer 10

Nausea and vomiting Agitation Confusion Dizziness Coma Metabolic acidosis and hyperglycaemia Peripheral vasodilation and severe hypotension (in dihydropyridine calcium channel blockers) Arrhythmias including heart block and asystole (Verapamil and diltiazem)

Answer 11

Nausea Vomiting Diarrhoea Abdominal pain Haematemasis Rectal bleeding Hepatocellular necrosis and hypotension can occur later Coma, shock and metabolic acidosis (in severe cases)

Answer 12

Most offten in patients on long-term lithium and whose excretion of lithium is reduced due to dehydration or infection etc Delayed onset of symptoms in deliberate overdose (12 hours or more) Initially: -apathy -restlessness Followed by: -vomiting -diarrhoea -ataxia -tremor -weakness -dysarthia -muscle twitching Severe poisoning: -electrolyte imbalance -dehydration convulsions -renal failure -hypotension -coma

Answer 13

Drowsiness Coma Respiratory depression Pinpoint pupils

Answer 14

Date of ingestion (any delay) Timing of ingestion (single or staggered) Time since last ingestion (staggered) Weight (max calc use 110kg) Pregnancy (use pre-pregnancy weight for toxicity and current weight for treatment) Total amount ingested (mg/kg) Current suicidal risk (consider MH assessment)

Answer 15

<75mg/kg are unlikely to cause toxicity unless staggered >150mg/kg are associated with serious or fatal adverse effects from toxicity Total doses >12g are potentially fatal

Answer 16

A potentially toxic dose of paracetamol taken within one hour or less

Answer 17

Excessive ingestion of paracetamol over a period longer than one hour, usually in the context of self-harm If time of ingestion is unknown then patients should be treated as a staggered overdose

Answer 18

Paracetamol is primarily metabolised in the liver to non-toxic metabolites but in overdose these pathways become overwhelmed Once ingested, paracetamol reaches peak conc at 4 hours within an average half life of 2 hours but this may be significantly increased in hepatic dysfunction patients Metabolism occurs via conjugation with the addition of glucuronide to form a water soluble metabolite that can be excreted in urine. In overdose the conjugation become saturated and paracetamol is instead converted into the metabolite N-acetyl-p-benzoquinoneimine (NAPQI) NAPQI has a short half-life and is usually conjugated by the addition of glutathione which is then renally excreted. If these stores are depleted then excess NAPQI binds to hepatocellular proteins and results in oxidative damage, mitochondrial dysfunction and hepatocellular injury.

Answer 19

(May increase the risk of severe hepatotoxicity) Fasting Excess alcohol consumption Certain drugs

Answer 20

Diagnosis based on history Investigations to assess for complications Hospital admission: -context of self harm -symptomatic -Ingestion of ≥75 mg/kg of paracetamol over an hour or less -Ingestion of ≥75 mg/kg but the time of ingestion is uncertain -Any patient who has taken a staggered overdose -Ingestion of more than the licensed dose (4g/24 hours for adults) and the total dose is ≥75 mg/kg within 24 hours, OR, <75 mg/kg within 24 hours for each of the preceding 2+ days. Bloods: -FBC -U and Es -LFTs -Bone profile -Venous/ arterial blood gas -Blood glucose -Paracetamol levels -Salicylates levels (always request in acute overdose)

Answer 21

Paracetamol ingestion graph used to determine if treatment with N-acetylcysteine (NAC) is needed Plots paracetamol concentration against time from ingestio, if the paracetamol conc lies on or above the treatment line, NAC should be administered. Used for patients who have ingested paracetamol over one hour or less and presented within 8 hours As plasma paracetamol conc reaches its peak at 4 hours, it is important to take a paracetamol within 4 hours of the last ingestion Start NAC in those with a delayed presentation; if paracetamol level will not be available within 8 hours from last ingestion; or staggered overdose

Answer 22

Prinicple treatment is N-acetylecysteine (IV) (NAC) NAC given as a standard 21 hour regimen which based on the patients weight It comprises three consecutive infusions: -First infusion (1 hour): 200ml 5% dextrose or 0.9% sodium chloride with 150 mg/kg of NAC -Second infusion (4 hours): 500ml 5% dextrose or 0.9% sodium chloride with 50mg/kg of NAC -Third infusion (16 hours): 1000ml 5% dextrose or 0.9% sodium chloride with 100mg/kg of NAC After the 21 hour regimen, blood tests are taken to look for any signs of hepatic impairment. If evidence of significant coagulopathy, deranged liver function tests or abnormal renal function - discuss with liver transplant centre. Can then give the third infusion of NAC continuously back to back until further advice.

Answer 23

Multiple proposed mechanisms of action Precursor to glutathione so administration increases the glutathione conc available to bind NAPQI Risk of anaphylactoid in 30% of patients on regimen, usually occurs after first infusion with features of nausea, comiting, urticarial rash, angioedema, tachycardia and bronchospasm (shock is uncommon) If adverse reaction happens, temporarily stop the infusion, consider chlorphenamine (antihistamine) and nebulised salbutamol. Once reaction has settled, restart the infusion - can consider slowing the rate of first bag to over 2 hours.

Answer 24

Same clinical picture to anaphylaxis but is not IgE-mediated

Answer 25

Acute ingestion (<8 hours ago) -consider activated charcoal -take paracetamol level at 4 hours -blood tests -nomogram -if above treatment level, start NAC Acute ingestion (8-24 hrs ago) -paracetamol level -bloods -Start NAC if dose >150mg/kg -Nomogram to help assess liver damage -At risk then continue NAC Acute ingestion (>24hrs ago) -paracetamol level -bloods -Start NAC if jaundiced or hepatic tenderness -Decision on NAC - continue if ALT raise or INR >1.3 or high paracetamol level -At risk then continue NAC Staggered overdose -Treat with NAC -Paracetamol level 4 hours after last ingestion -Blood tests -If at risk, continue NAC

Answer 26

At the end of the standard 21-hour infusion of NAC, patients need to undergo repeat blood tests for LFTs, U&Es, INR and venous blood gas. Treatment may be stopped when: -INR ≤1.3 and ALT within normal range, OR -INR ≤1.3 and ALT raised but <2x upper limit of normal and not more than double admission ALT Treatment with NAC should be continued when: -ALT >2x upper limit of normal -ALT is raised and more than double the admission ALT -ALT is raised and INR >1.3 (in absence of another cause) -INR >0.5 from admission value

Answer 27

Occurs when there is inadequate gaseous exchange in the lungs it is defined by the partial pressure of O2 and CO2 in the arterial blood Two types: -Type 1 respiratory failure: is characterised by hypoxaemia (PaO2 < 8 kPa) and a normal or low CO2. -Type 2 respiratory failure: is characterised by hypoxaemia (PaO2 < 8 kPa) and hypercapnia (PaCO2 > 6.5 kPa).

Answer 28

Hypoxaemia is most commonly caused by a V/Q mismatch Hypercapnia is often caused by alveolar hypoventilation Number of process can lead to hypoxaemia and hypercapnia

Answer 29

Ventilation to perfusion ratio The ratio of alveolar ventilation to alveolar perfusion In the average adult they are ventilated by 4L of air and perfused by. 5L of blood each minute, giving V/Q ratio of 0.8 (4:5) There is normal for mismatch in V/Q to differ depending on the part of the lung eg better perfusion at the bases than the apices due to gravitational and hydrostatic forces; ventilation is also greater in the same way but to a lesser extent. In disease, there may be an increase in the V/Q mismatch leading to hypoxaemia Low V/Q refers to alveolar units with poor ventialation compared with perfusion resulting in hypoxaemia due to low alveolar o2 levels. May be seen in airway disease or interstitial lung disease where ventilation is reduced High V/Q refers to alveolar units with poor perfusion compared with ventilation. This occurs in areas where perfusion is limited eg PE. The hypoxaemia in V/Q mismatch normally responds well to O2 therapy by improving alveolar oxygenation in low V/Q areas

Answer 30

Refers to blood entering the left side of the heart without first having travelled through pulmonary capillaries and participating in gaseous exchange This can be thought of as an extreme version of V/Q mismatch (V/Q=0) Shunts respond relatively poorly to oxygen therapy when compared to v/q mismatch as the shunted blood cannot be ventilated. Hypercapnia may occur if there is a high shunt fraction.

Answer 31

Pneumonia ARDS Pulmonary oedema Alveolar collapse

Answer 32

The impairment of gaseous exchange across the alveolocapillary membrane Can occur by: -Reduced surface area of alveoli due to pathological destruction limiting the amount of lung tissue available for gaseous exchange -Alveolcapillary membrane changes by inflammation and fibrosis, impairing diffusion across the membrane Often seen in emphysema and lung fibrosis Hypercapnia is less common than hypoxaemia as carbon dioxide is far more soluble and less likely to be affected The hypoxaemia normally resonds well to O2 therapy

Answer 33

Dead space represents areas of the lung that are ventilated but not perfused and therefore do not contribute to gaseous exchange An extreme V/Q mismatch but the opposite of a shunt (V/Q=infinity, technically undefined) Dead space can be: -Anatomical - in the conducting airways where no gas exchange takes place -Alveolar - caused by alveoli that are ventilated but not perfused -Physiological - a combination of anatomical and alveolar

Answer 34

Through destruction of pulmonary capillaries Seen in: -Emphysema (COPD) -Interstitial lung disease Results in a lower proportion of tidal volume engaging in gaseous exchange and leads to hypercapnia

Answer 35

Characterised by hypoxaemia (PaO2 <8kPa) and a normal or low paCO2 Most commonly caused by V/q mismatch, but is also seen in shunts, diffusion limitationa dn alveolar hypoventilation Can be acute or chronic

Answer 36

Polycythaemia (an increase in red cell mass in the blood) Development of cor pulmonale

Answer 37

Pneumonia COPD Asthma Pulmonary oedema Pneumothorax PE Obesity

Answer 38

Characterised by hypoxaemia (PaO2 <8kPa) and hypercapnia (PaCo2>6.5kPa) AKA hypercapnic respiratory failure Seen in conditions that result in alveolar hypoventilation Can be acute or chronic depending on speed of onset and presence of compensatory mechanisms

Answer 39

Can present with significant hypoxaemia, electrolyte disturbances, cardiovascular instability, loss of consciousness and ultimately cardiac arrest. It is usually indicated by an acute insult (eg opiate overdose or acute exacerbation of COPD) with a new respiratory acidosis and no evidence of chronic compensation (eg normal bicarbonate)

Answer 40

Exacerbations of obstructive lung disease: -COPD -Severe asthma -Cystic fibrosis -Bronchiectasis Respiratory depressants -Opiate overdose

Answer 41

Evidenced by compensatory mechansisms seen on ABGs (or VBGs) Increase in the Bicarbonate level occurs in the setting of chronic resp acidosis (can be in 30s when normal is 22-26) Chronic resp acidosis may be fully compensated with a normal pH, elevated paCO2 and significantly elevated bicarbonate level

Answer 42

COPD Asthma Chronic neurological disorders (eg motor neuron disease) Chronic neuromuscular disorders (eg myopathies) Chest wall diseases Obesity hypoventilation syndrome

Answer 43

It is now understood that the development of oxygen-induced hypercapnia is multifactoral: -Increased V/Q mismatch: increased O2 administration impairs hypoxic pulmonary vasoconstriction and results in increased V/Q mismatch and physiological dead space. -Haldane effect: the presence of oxygen causes haemoglobin to have a reduced affinity for CO2. This results in CO2 being displaced from haemoglobin increasing the PaCO2. -Decreased minute ventilation (less important than the above two factors) COPD patients who are CO2 ‘retainers’ should generally have a lower saturation target of 88-92%.

Answer 44

Group of medications of which aspirin is the most common There are all NSAIDs and have a dual action as an antiplatelet at lower doses and an analgesic at higher doses

Answer 45

Mild toxicity: -irritate gastric lining -ototoxicity through multifactorial process involving reduced cochlear blood flow, secondary to vasoconstriction and changes to cochlear cells Moderate/ severe toxicity: -mixed respiratory alkalosis and metabolic acidosis -stimulate the cerebral medulla, leading to hyperventilation and respiratory alkalosis -metabolism of salicylates causes uncoupling of oxidative phosphorylation, resulting in anaerobic metabolism, causing heat production and pyrexia and increased lactic acid production, resulting in metabolic acidosis. The acidic effects of salicylates also contribute to the associated acidosis -hyperventilation worsens in response to the acidosis until the body can no longer compensate

Answer 46

Mild: -Nausea and vomiting -Epigastric pain -Tinnitus -Dizziness -Lethargy Moderate: -Sweating -Fever -Dyspnoea Severe: -Confusion -Convulsions -Coma

Answer 47

Warm peripheries Bounding pulse Tachypnoea Hyperventilation Cardiac arrhythmia Acute pulmonary oedema

Answer 48

Bed side obs ECG - arrhythmias, QRS duration, QT prolongation Cap glucose - to exclude hypo/hyper glycaemia ABG- monitor acid base balance, initially hyperventilation will cause resp alk but then progress to met acidosis with partial resp compensation with normal or high pH Plasma salicylate conc - >2 hours after ingestion and repeat every 2 hours till peaks Plasma paracetamol conc in those with mixed overdose FBC - exclude infection U and Es - hyperkalaemia common, urea and creatinine may be raised, indicating AKI LFTs - assess hepatic dysfunction Coagulation - INR and prothrombin time may be increased in hepatic dysfunction CT head - if altered mental state and intracranial pathology is suspected

Answer 49

TOXBASE classifies overdose as mild, moderate or severe based on clinical features and peak salicylate levels Mild toxicity: <300 mg/L Moderate toxicity: 300 to 700 mg/L Severe toxicity: >700 mg/L

Answer 50

A to E No antidote so simply supportive care ICU admission to be considered in moderate to severe toxicity Initial management: -Activated charcoal - if presenting within 1 hour of >125mg/kg ingestion -IV fluid resuscitation - if volume depleted -Potassium replacement - urgent hypokalaemia treatment with IV infusion to maintain plasma potassium at 4-4.5 mmol/L. Sodium bicarbonate therapy can precipitate hypokalaemia so any pre-existing hypokalaemia should be urgently corrected -Sodium bicarbonate - reduces transfer of salicylates into the central nervous system and enhances urinary excretion of salicylates (aka urinary alkalinisation). Monitor urine pH (optimal 7.5-8.5). Ongoing management: -Cooling measures -Haemodialysis - treatment of choic in severe salicylate poisoning with renal failure, severe metabolic acidosis or seizures -IV Benzodiazepines - if frequent or prolonged convulsions -CPAPA - if pulmonary oedema or acute lung injury, secondary to salicylate overdose -Psychological support - if intential overdose

Answer 51

Haemodialysis involves the diffusion of solutes from a high concentration to a low concentration across a semipermeable membrane. Haemofiltration uses convection and high pressure to force solutes from the blood to the dialysis fluid for disposal. Haemodiafiltration combines the two processes.

Answer 52

Acute respiratory distress syndrome (ARDS) Seizures Drug induced hepatitis Cardiac arrest

Answer 53

Acute respiratory distress syndrome (ARDS)

Answer 54

A class of meds developed for severe depression but often now used for neuropathic pain and migraine prophylaxis

Answer 55

Amitriptyline Nortitiptyline Dosulepin

Answer 56

Prevents the neurotransmitter from being transported back into the pre synaptic neurone once released into the synaptic cleft and so the neurotransmitter sontinues to activate the postsynaptic receptor, increasing its effect

Answer 57

Prevents the neurotransmitter from activating the postsynaptic receptor overall reducing its effect

Answer 58

Reuptake inhibition (increased effect): -Serotonin (5-HT receptors) -Noradrenaline (NA receptors) Postsynaptic receptor antagonism (decreased effect) -Histamine (H1 receptors) -A-1 adrenoreceptors -Acetylcholine receptors

Answer 59

Clinical manifestations of overdose become apparent within 6 hours of ingestion Symptoms: -dry mouth -hot, dry skin -confusion and hallucinations -palpitations Severe effects: -arrhythmia -cardiovascular collapse -convulsions -coma A to E A - risk of airway compromise B - respiratory depression C - myocardial sodium channel blockade resulting in hypotension and arrhythmias; serotenergic activity can causes tachycardia and peripheral vasodilation; ECG findings of widened QRS and prolonged QTc which predisopose to ventricular tachcardia and ventricular fibrillation D - confusion, seizures and coma; check glucose too E - hyperthermia due to serotenergic effects; anticholinergic signs including dry skin, eyes and mouth, urinary retention and ileus

Answer 60

Potentially life threatening presentation Overactivation of both central and peripheral serotonin receptors Caused by serotonergic drugs (eg TCAs, SSRIs, some opioids) Features: -altered mental state -neuromuscular hyperactivity -autonomic hyperactivity Clinical presentations: -hyperntension -tachycardia -diaphoresis -myoclonus -hyperreflexia -hyperthermia (severe cases) -muscle rigidity (severe cases) Clinical diagnosis with supportive management

Answer 61

Bedside: -Obs (tachycardia, hypotension, hyperthermia) -12 lead ECG (widened QRS and prolonged QTc, risk of VF and VT) -Blood glucose (exclude hypoglycaemia) -Blood gas (mixed acidosis - treat with bicarbonate) Laboratory: -FBC (base line) -U and Es (hypokalaemia, renal impairment hx) -Magnesium and bone profile (electrolyte disturbances can worsen arrhythmias) -LFTs (in co-ingestion) -Paracetamol and salicylate levels (checked in all with overdose especially in unclear history) Imaging: -No sepcific imaging but may be useful to do: -CXR (in reduced consciousness level and airway compromise) -CT head (should be considered in patients with significantly reduced GCS to rule out concurrent intracranial pathology. Also in those presenting with seizures)

Answer 62

No specific antidote, so supportive management Activated charcoal can be given to the conscious patient to prevent absorption if they present within one hour of ingestion Sodium bicarbonate can be given in arrhythmia and acidosis to prevent progression to ventricular arrhythmias A to E A- airway manoeuvres or adjuncts or intubation is need definitive airway management B- high flow O2 and start SpO2 monitoring C- IV access, continuous cardiac monitoring in all unwell patients or those with an abnormal initial ECG, administer fluid bolus to hypotensive patients and sodium bicarbonate if cardiac arrhythmias occur D- assess and monitor consciousness, Benzodiazepines should be given for seizures, phenytoin should be avoided due to its serotenergic effects E- cooling measures for hyperpyredia, manage other symptoms as they develop (eg catheterise in urinary retention) Mental health assessment required in intentional overdose

Answer 63

If left untreated can result in death secondary to cardiac or neurological effects. Prolonged seizure activity can result in brain injury and coma Those with reduced consciousness are at risk of aspiration pneumonia if there airway is not managed effectively.

Answer 64

Local GI effects followed by systemic effects (that do not occur without preceding GI toxicity following iron ingestion) Local: -corrosive injury to GI mucosa resulting in: -- vomiting -- diarrhoea -- haemetemesis -- melaena -- fluid loss which may result in hypovolaemia Systemic: -exact mechanisms are uncertain -iron acts as a cellular toxin targeting the CV system and the liver, with secondary CNS effects, metabolic acidosis due to hyperlactaemia and free proton production from the hydration of free ferric ions, and coagulopathy Overwhelms the normally regulated GI absorption of iron and bioavailability is greatly increased Once absorbed, gradually mvoed intracellularly over 6 to 12 hours Elimination is minimal

Answer 65

<20mg/kg – asymptomatic 20-60mg/kg – GI symptoms only 60-120mg/kg – potential for systemic toxicity >120mg/kg – potentially lethal Note that this is based on the amount of elemental iron ingested. This varies considerably between different types of iron tablets, depending on the type of ferrous or ferric salt: ferrous sulfate (dried) - divide dose by 3.3 ferrous sulfate (heptahydrate) - divide dose by 5 ferrous gluconate - divide dose by 9 ferous fumarate - divide dose by 3 ferric chloride - divide dose by 3.5 ferrous chloride - divide dose by 4

Answer 66

Follows 5 stages: 0-6 hours – vomiting, diarrhoea, haemetemesis, melena, abdominal pain. Significant fluid loseses may lead to hypovolemic shock 6-12 hours – gastrointestinal symptoms wane and the patient appears to be getting better. During this time iron shifts intracellularly from the circulation 12-48 hours – Cellular toxicity becomes manifest as vasodilative shock and third-spacing, high anion gap metabolic acidosis (HAGMA) and hepatorenal failure 2-5 days – acute heaptic failure, although rare mortality is high 2-6 weeks – chronic sequelae occur in survivors – cirrhosis and gastrointestinal scarring and strictures

Answer 67

In addition to the usual screening tests in suspected tox cases (BSL, ECG, paracetamol level) the following specific tests can be useful: serum iron concentration -peak levels occur 4-6 hours following iron ingestion -after 6 hours iron levels fall due to intracellular shift -levels do not clearly correlate with clinical toxicity, but > 90 micromol/L (500 mcg/dL) is generally considered predictive of systemic toxicity (equivalent to >60mg/kg) blood gas -the presence of HAGMA is a useful marker of systemic toxicity -in the absence of iron levels a serum bicarbonate level can be used as a surrogate marker abdominal X-ray — can be used to confirm ingestion LFTs, Coags — hepatic failure UEC — renal failure

Answer 68

Resuscitation as indicated with concurrent specific assessment and management of the toxidrome. Resuscitation: -ABCs -Priority is early restoration of circulating volume -Resuscitate with boluses of 10-20 mL/kg crystalloid to prevent shock from gastrointestinal losses, vasodilation and third spacing Supportive care and monitoring -Ongoing assessment of response to resuscitation and antidotes Decontamination: -Iron not adsorbed by activated charcoal -Whole bowel irrigation indicated for confirmed ingestions > 60 mg/kg (difficult and potentially hazardous in small children) -Surgical or endoscopic removal of tablets if lethal ingestion (e.g. >120mg/kg) or WBI not feasible Antidotes: -Desferrioxamine chelation therapy in cases of systemic toxicity (high serum 1iron level or metabolic acidosis on ABG) Disposition: -Ingestion of >40/mg/kg in children should be assessed at hospital -Those asymptomatic at 6 hours with a negative abdominal x-ray can be discharged home -Those with symptoms are admitted to hospital and may require IV fluids (ward, HDU, ICU depending on severity; ideally a paediatric center) -Patients with the potential for systemic toxicity may be best managed at larger hospitals where iron levels can be measured and iron chelation therapy administered if needed -Consider neglect in children -Psychiatric assessment in adults DESFERRIOXAMINE

Answer 69

An option for severe iron toxicity – the indications, duration and end-points of therapy are controversial. Indications (may also be used in chronic iron overload) -level >90 micromol/L at 4-6 hours post-ingestion -evidence of systemic toxicity -shock -metabolic acidosis -altered mental status Mechanism of action -chelates free ferric and ferrous ions in the plasma resulting in water soluble complexes that can be renally excreted -removes iron bound to transferrin and hemosiderin in the vascular compartment (does not effectively remove iron from stores in other compartments) -ferrioxamine is excreted unchanged in the urine, which classically turns a vin rose colour (although this is not a reliable indicator of chelation) Administration -initial IV infusion rate of 15 mg/kg/h, reduced if hypotension occurs, may be titrated up to 40mg/kg/h in severe toxicity -cardiac monitoring is mandatory -reconstitute the 500 mg powder with 5 mls sterile water and dilute to 100 mls with 5% glucose or normal saline Adverse effects -hypersensitivity -hypotension (with rapid or high-dose IV administration) -ARDS (with infusions >24h) -toxic retinopathy -Yersinia sepsis (the ferrioxamine complex is a siderophore that promotes growth) Endpoints -The infusion can be stopped when the patient is clinically stable and the serum iron level is <60 micromol/L -usually about 56 hours therapy is sufficient -treatment >24 hours is rare

Emergency Conditions Flashcards

(93 cards)