Acute Flashcards

Question

Prognosis of ARDS

Answer 1

Mortality in patients who develop ARDS is 30% to 50%. Death is most often due to multiple organ failure rather than purely to respiratory failure. Muscle weakness, neuropathies, joint disorders, and chronic pain are also common in survivors of ARDS at 1 year.

Answer 2

``` Death Ventilator associated pneumonia Multiple organ failure Pneumothorax Persistent dyspnoea Abnormal lung function Decreased QOL ```

Answer 3

Asymptomatic patients, who meet none of the above criteria for inpatient management, may be considered for observation at home for 12 to 24 hours. Rx: 1) activated charcoal: children: 1 g/kg orally as a single dose; adults: 50-100 g orally as a single dose 2) serum and urinary alkalisation - sodium bicarb 3) emergency haemodialysis Inducing emesis is not indicated for salicylate ingestions. The first step in treating any patient with suspected poisoning or overdose presenting to the hospital accident and emergency department (A&E) is to ensure airway patency and adequate breathing and circulation. Hydration should be addressed and any electrolyte abnormalities corrected as soon as possible. Patients are frequently volume-depleted at time of presentation. Two intravenous lines should be placed (one in each arm) in order to begin adequate rehydration and to initiate alkalinisation if needed.

Answer 4

Risk of death and serious toxicity from acute ingestion increases with increasing interval between ingestion and treatment. One study showed that substantial morbidity and mortality increased if the estimated interval between ingestion of large amounts of salicylate and treatment exceeded 12 hours

Answer 5

ARDS Cardiac arrest Seizures Drug-induced hepatitis

Answer 6

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 chemicals. Severity is assessed by burn size (% total body surface area) and depth (first to fourth degree). Most burns can be managed in an outpatient setting. Early management affects long-term outcome. Initial treatment of minor burns consists of wound cooling, cleaning, and dressing. Pain management and tetanus prophylaxis are important. Serious burns are most effectively managed in regional burn centres. Prognosis varies from excellent to poor depending on the severity of the burn. Associated injuries (such as inhalation injury or trauma) adversely affect the prognosis. The majority of patients will have satisfying outcomes.

Answer 7

250,000 people are injured by burns. Approximately 175,000 people visit accident and emergency departments with burn injuries. Around 13,000 of them are admitted to hospital for treatment.

Answer 8

STRONG Young children Age >60years Male sex

Answer 9

``` COMMON RFs 1st deg Erythema 2nd deg Dry and painful burns 3rd deg Wet and painful 4th subcutaneous tissue/tendon/bone Cellulitis Clouded cornea ```

Answer 10

FBC - may show low haematocrit, hypovolaemia, neutropenia, thrombocytopenia Metabolic panel - may show high levels of urea, creatinine, glucose; hyponatraemia, hypokalaemia Carboxyhaemoglobin - Indicated if inhalation injury is suspected. ABG - may show metabolic acidosis in inhalation injury Flourescein staining - damaged corneal epithelial cells in corneal burns Wound biopsy culture - if suspect infection Wound histology - may show wound infection

Answer 11

SUITABLE FOR OUTPATIENT CARE: Silver is an excellent antiseptic and is used in burn wound care in several forms, including silver sulfadiazine cream, aqueous silver nitrate solution, and dressings containing nanocrystalline silver. Clean burn wounds with lukewarm tap water and a bland soap. Tetanus immunisation Opioid analgesic ABx / surgical debridement if needed REQUIRES INPATIENT CARE - Fluid resus - O2 and supportive care - Tetanus immunisation - Surgery - DVT prophylaxis - Opioid and benzo pain + anxiety - May need Abs and debridement - SURGERY: Temporary wound membranes can be useful in patients with large wounds.

Answer 12

``` Sepsis Pneumonia Intubation related Chondritis Hepatic dysfunction Acalculous cholecystitis Gastroduodenal ulceration UTI Transient delirium Seizures Acute renal failure Acute adrenal insufficiency Endocarditis Thrombophlebitis DVT Intestinal ischaemia Corneal abrasion Compartment syndrome Hypertension Hypertrophic scarring Heterotopic ossification Marjolin ulcer Resp failure Hepatic failure Pancreatitis Nerve injury Post traumatic stress disorder ```

Answer 13

It can vary from excellent to poor depending on the severity of the burn. Most burns are minor and the prognosis in these patients is excellent; however, major burns can be fatal.

Answer 14

Adrenal suppression refers to decreased cortisol production as a result of negative feedback on the hypothalamic-pituitary-adrenal axis, caused by excess glucocorticoids. The consequence is decreased production of both corticotropin-releasing hormone from the hypothalamus and adrenocorticotropic hormone from the pituitary gland, leading to a decrease in serum cortisol levels. Pathophysiology involves suppression of the hypothalamic-pituitary-adrenal axis. Symptoms may be related to rapid tapering or cessation of exogenous glucocorticoids (resulting in a form of secondary adrenal insufficiency) or withdrawal from endogenous glucocorticoid excess (e.g., Cushing's syndrome after treatment). Even locally administered glucocorticoids may result in adrenal suppression. The adrenocorticotropic hormone stimulation test is generally the most useful test to detect adrenal suppression. Treatment consists of augmented corticosteroid therapy plus supportive care for any intercurrent stress or overt signs of adrenal insufficiency. Preventive measures include minimising corticosteroid dose and duration when possible.

Answer 15

Adrenal suppression is most commonly encountered in patient populations where an underlying disease is treated with exogenous glucocorticoids (e.g., chronic obstructive pulmonary disease, asthma, or arthritis). The prevalence or incidence of adrenal suppression in these different subpopulations is not often reported but may be more common than generally believed. In a cohort of 48 controls and 16 paediatric patients with asthma given beclometasone dipropionate at a dosage of 300 to 500 micrograms daily, the baseline risk of adrenal suppression was 0% before and 100% after treatment for 6 to 42 months, as documented by insulin tolerance test.

Answer 16

``` Systemic glucocorticoid administration High potency or dose of exogenous glucocorticoids Local glucocorticoid administration Glucocorticoid treatment >3w Megestrol use ``` WEAK Non-physiological scheduling of glucocorticoid dose Medroxyprogesterone use

Answer 17

``` Sudden reported cessation Hx weight gain + increased appetite Hx depression, agitation, sleep disorders, easy bruising N+V Fatigue anorexia WL Dizziness/orthostatic Myalgia + arthralgia Abdominal pain Cushingoid examination features Patients may have moon facies, facial plethora, dorsocervical fat pad, bruising, violaceous abdominal striae, thin skin, proximal muscle weakness, and centripetal obesity. ``` Absence of hyperpigmentation or autoimmune stigmata Hypotension with or without orthostasis

Answer 18

U+E - possible hypo- or hyperglycaemia, hypokalaemia, hypomagnesaemia, contraction alkalosis 9am cortisol - <110 nanomol/L (4 micrograms/dL): likely adrenal insufficiency Salivary AM cortisol - <414 nanomol/L (<0.15 micrograms/dL): likely adrenal insufficiency ACTH stimulation test - synACTHen - rise of cortisol to an absolute level >497 nanomol/L (18 micrograms/dL) excludes adrenal insufficiency

Answer 19

ADRENAL CRISIS 1. Stress dose hydrocortisone - hydrocortisone sodium succinate: 50-100 mg intravenously every 6-8 hours 2. Supportive - Intravenous fluids in the form of 5% dextrose in normal saline should be given to address the volume depletion that is often present. 3. A search for the condition that precipitated the crisis, such as infection, should be undertaken. Treatment of the underlying cause should be instituted. 4. Taper dose ___________________ MINOR STRESS 1. Temporary double dose of existing corticosteroid CONSULT EXPERT for surgical stress doses

Answer 20

Adrenal insufficiency secondary to corticosteroid treatment has a generally good prognosis. Time to recovery depends on dose and/or potency of glucocorticoid used and treatment length. Signs and symptoms of Cushing's syndrome will disappear with time as the inciting medication is stopped.

Answer 21

Corticosteroid dependence | Permanent sequelae of adrenal crisis

Answer 22

adrenal suppression Patients may or may not appear cushingoid. When the inciting medication or condition is suddenly removed, secondary adrenal insufficiency occurs. Signs and symptoms of corticosteroid-induced adrenal suppression may be subtle or overt. Symptoms range from vague fatigue and nausea to those of adrenal crisis (e.g., hypotension).

Answer 23

Carbon monoxide (CO) poisoning can occur following exposure to a variety of sources. The increased affinity of CO with haemoglobin results in tissue hypoxia and impairment of cellular respiration, and direct effects of CO toxicity at the cellular level. The symptoms of CO poisoning can be acute or chronic, depending on dose and duration of the exposure. They are mostly non-specific, and vary from headache, nausea, and dizziness to severe cardiovascular and neurological symptoms. People who are most at risk of having adverse outcomes after CO poisoning are those with coronary heart disease, vascular disease, or anaemia; pregnant women and their fetuses; infants; and older people. About one third of severe poisonings are fatal. Carbon monoxide (CO) is an odourless, colourless gas, and poisoning can cause hypoxia, cell damage, and death. Approximately one third of severe poisonings are fatal. Poisoning can occur following exposure from fire or non-fire sources. Early symptoms are non-specific and include headache, dizziness, and nausea. Increasing exposure results in cardiovascular effects such as myocardial ischaemia, infarction, dysrhythmias, and cardiac arrest. Neurological symptoms include acute stroke-like symptoms, altered mental status, confusion, coma, and syncope. Diagnosis is based on the history, carboxyhaemoglobin levels and the patient’s symptoms. High-flow oxygen therapy, hyperbaric oxygen, and supportive therapy are the key treatments for CO poisoning. Complications of hyperbaric treatment include seizures related to oxygen toxicity, barotraumas, and pulmonary oedema.

Answer 24

In the UK, 50 people are killed and nearly 200 seriously injured as a result of CO poisoning each year. Exposure to CO may be accidental or intentional. The highest mortality in the US has been reported among males, and black and older people. There is a seasonal predominance with higher rates of death reported in winter.

Answer 25

A variety of sources generate CO, including internal combustion engines, water heaters, and home heating units. Kerosene space heaters were responsible for CO poisoning in the 1970s. Other sources of CO exposure are the paper mill industry, steel mills, explosives used in construction, petroleum refineries, and petrol-powered machinery. CO is formed during metabolism of methylene dichloride (dichloromethane). Exposure to CO during paint or furniture stripping and de-greasing may result in poisoning.

Answer 26

``` presence of risk factors nausea headache vomiting blurred vision dizziness cutaneous blistering tachycardia hypotension cardiac arrhythmias pulmonary oedema confusion coma ``` seizures focal neurological abnormalities (e.g., hemiplegia)

Answer 27

CO-Hb level - toxic effects appear at 15% to 20%, severe poisoning occurs at 25% CXR - signs of non-cardiogenic pulmonary oedema ECG - tachycardia, arrhythmias, features of cardiac ischaemia Cardiac monitoring BG - Neurological outcomes following CO poisoning are worse in patients with hyperglycaemia. Lactate - may be elevated in severe poisoning Cardiac biomarkers - may be elevated

Answer 28

1. Supportive - It is recommended to monitor lactate to estimate metabolic acidosis, blood glucose to eliminate hypoglycaemia as a cause for altered mental status, and creatine kinase to monitor for rhabdomyolysis. An ECG and cardiac markers may be monitored to detect evidence of end-organ damage.Carboxyhaemoglobin can also be monitored, although levels may be low in patients receiving oxygen. Fetal monitoring is necessary in pregnant women to detect any evidence of fetal distress or fetal compromise. + high flow o2 2. Hyperbaric O2 therapy - Indicated in patients with neurological findings such as altered mental status, coma, focal neurological deficits, or seizures, or a history of prolonged unconsciousness, cardiovascular dysfunction, or severe acidosis, or pregnant women with carboxyhaemoglobin levels >15%. 3. Neurological outcomes following CO poisoning are worse in patients with hyperglycaemia.[17] Therefore, consider giving insulin to patients if blood glucose levels are high and titrate treatment to avoid dangerously low levels of blood glucose.

Answer 29

``` Barotrauma 2nd to hyperbaric O2 MI Seizures - hyperB Rx Complications secondary to O2 therapy - pulmonary complications of oxygen toxicity include reduced vital capacity, pulmonary fibrosis, ARDS, and impaired gas exchange. Fire accidents Delayed neurological sequelae Memory deficit Personality changes Rhabdomyolysis ```

Answer 30

There are no clear data on prognosis following CO poisoning. Approximately one third of severe poisonings are fatal. Factors that indicate poor prognosis are advanced age, acidotic states, pre-existing cardiovascular disease, and structural abnormalities on imaging studies such as lucencies in the basal ganglia, cerebral white matter and globus pallidus. Even mild symptoms in a pregnant woman can have devastating effects on the unborn child, such as fetal demise or congenital malformations. Fetal haemoglobin has a much greater affinity for CO than adult haemoglobin.

Answer 31

Carbon monoxide poisoning Other less common clinical presentations of CO poisoning include rhabdomyolysis, acute renal failure from muscle damage, skin bullae, and non-cardiogenic pulmonary oedema. Children can present with non-specific symptoms mimicking viral illness such as nausea and vomiting, but fever and other symptoms of infection are usually absent. Delayed effects can be seen up to 6 weeks after exposure and include confusion, ataxia, hallucinations, and motor and gait disturbances. Long-term exposure to low levels of CO can cause anorexia, personality disorders, acceleration of atherosclerosis, and polycythaemia and cardiomegaly due to chronic hypoxia.[3] Even mild symptoms in a pregnant woman can have devastating effects on the unborn child, such as fetal demise or congenital malformations. Fetal haemoglobin has a much greater affinity for CO than adult haemoglobin.

Answer 32

A hip fracture is generally considered to be any fracture of the femur distal to the femoral head and proximal to a level a few centimetres below the lesser trochanter. Occurs predominantly in the elderly. The risk increases significantly with age. Associated most commonly with low-energy injury (e.g., fall from standing height) and osteoporosis or osteopenia. Treatment is most commonly surgical. The choice of implant depends on the fracture pattern and the surgeon's preference.

Answer 33

Projected lifetime risk of sustaining a hip fracture is 11.1% for men and 22.7% for women. The risk of hip fractures increases significantly with age, and they are more frequent in those more than 65 years of age, with the average age being approximately 78 years. The predominant mechanism of injury is a fall from a standing height.

Answer 34

STRONG ``` Osteoporosis/penia >65 Falls Low BMI Female Sex High-energy trauma ```

Answer 35

COMMON Inability to ear weight Pain in affected hip/leg: Pain in the groin or proximal femur is often increased with internal or external rotation of the leg or flexion of the hip. Pain with hip movement Shortened + externally rotated leg

Answer 36

Plain Xray Consider: MRI pelvis CT pelvis Technetium bone scane

Answer 37

INTRACAPSULAR + UNDISCPLACED: - Internal fixation - Treatment in most instances is internal fixation with a dynamic hip screw or multiple cannulated screws. Prophylactic ABx Morphine sulfate 5-10mg IV 4hr REHABILITATION INTRACAPSULAR DISPLACED: Internal fixation OR arthroplasty Current best evidence suggests that total hip arthroplasty may reduce pain and functional limitation more than hemi-arthroplasty. However, this may come at the cost of a slightly higher risk of hip dislocation with total hip arthroplasty. EXTRACAPSULAR / INTERTROCHANTERIC FRACTURE displaced or undisplaced Treatment in most instances is internal fixation with dynamic hip screw or cephalomedullary nail. Current best evidence suggests that dynamic hip screws are the preferred method of treatment for inter-trochanteric fractures, with some meta-analyses suggesting a decreased complication rate and re-operation rate.

Answer 38

Thromboembolic complications Avascular necrosis - Risk increases if the femoral neck fracture is displaced. Non-union / failure

Answer 39

Hip fractures carry an approximately 30% risk of mortality at 1 year, and 25% to 75% of community-dwelling adults may not regain their pre-fracture level of function. Predictors of mortality include significant comorbid disease, low pre-injury cognitive function, abnormal pre-operative ECG, age >85 years, and decreased pre-fracture mobility. Operating within 48 hours has been shown to be beneficial.

Answer 40

hip fracture Usually occurs in patients more than 65 years of age or in those who have osteopenic conditions of bone or osteoporosis. They are generally due to low-energy injuries in this patient group. However, hip fractures may present in those younger patients with high-energy injuries such as motor vehicle accidents and falls from height; these fractures can then be associated with other fractures of the femur and other injuries consistent with poly-trauma.

Answer 41

Neuroleptic malignant syndrome (NMS) is an uncommon, idiosyncratic, life-threatening complication of treatment with antipsychotic medications. NMS has also been associated with other psychotropic agents that block central dopamine pathways (e.g., metoclopramide). It is characterised by altered mental state, increased muscle tone or frank rigidity, alterations in the autonomic nervous system, hyperactivity, and hyperthermia. None of these signs are exclusive to this condition, and other important diagnoses (e.g., sepsis) should be excluded first. A serious, potentially life-threatening complication of treatment with antipsychotic drugs or abrupt withdrawal of dopamine agonists. Characterised by a tetrad of altered mental status, muscle rigidity, autonomic instability, and hyperthermia. A diagnosis of exclusion. Common differential diagnoses are sepsis and drug reactions. NMS is a medical emergency. Treatment consists of immediate cessation of the offending medication and provision of supportive measures (hydration and cooling). Additional treatment may be considered if supportive interventions fail. A delay of at least 2 weeks in restarting antipsychotic treatment after an NMS episode has fully resolved is advised. Documenting this reaction in the medical records is important.

Answer 42

NMS has been reported to be more common in male than in female patients, but larger studies have not consistently found this. Pre-existing structural brain abnormality, catatonia, and older age are associated with an increased risk. 8% mortality

Answer 43

STRONG Exposure to antipsychotic medications Abrupt withdrawal of dopaminergic drugs Structural brain abnormality WEAK ``` Older age Pre-existing agitation Akathisia Male Iron Deficiency Catatonia Pre-existing dehydration Exposure to other dopamine antagonists ```

Answer 44

``` Altered mental state Muscle rigidity Autonomic dysfunction - Tachycardia, labile hypertension, diaphoresis, tachypnoea, urinary incontinence. Hyperthermia Psychiatric Hx Hx IDA Hx Wilsons disease ```

Answer 45

FBC - WBC count may be elevated Serum CK - high levels (>500 units/L); levels above 180,000 units/L have been reported Basic metabolic panel - usually normal in NMS Brain CT - usually normal in NMS; may reveal potential structural brain abnormality Brain MRI - usually normal in NMS; may reveal potential structural brain abnormality Myoglobin + urinalysis - Myoglobinuria is a poor prognostic sign because it may herald multi-organ failure. Urine culture - To exclude sepsis. Blood culture - To exclude sepsis. Lumbar puncture - To exclude sepsis. Toxicology screen - To rule out drug abuse/overdose (e.g., ecstasy). CxR - To exclude pneumonia. Some patients with NMS are at increased risk for aspiration. CONSIDER Serum iron - Acute, transient low levels have been described, and in some cases appear to signal imminent worsening. EEG

Answer 46

If NMS is suspected, antipsychotics and dopamine antagonists must be stopped, and dopamine agonists must be restored or continued. Other drugs that may be contributory (e.g., lithium) may need to be stopped. Most patients are dehydrated in the acute phase of the illness; therefore, administration of fluids and monitoring and correction of electrolyte abnormalities are essential. When rhabdomyolysis occurs, vigorous hydration with intravenous fluids is recommended to prevent acute kidney injury. Hyperthermia can be treated with physical cooling measures; antipyretics such as paracetamol or ibuprofen do not appear to be effective in NMS. Patients with dysphagia might require a nasogastric tube for the administration of fluids, nutrition, and pharmacological therapy ``` PHARMACOLOGICAL: Lorazepam 1-4mg Dantrolene Bromocriptine 2.5-5mg Amantadine - 200-400mg 2 divided doses ```

Answer 47

8% MORTALITY Recurrence of NMS has been estimated to be as high as 30%, but there are no reliable data regarding recurrence. It is usually recommended that rechallenge be postponed until at least 2 weeks after complete resolution of the syndrome. Rechallenge should proceed slowly and under close monitoring, including appropriate laboratories.

Answer 48

``` Sepsis AKI Rhabdo PE Aspiration Cognitive deficits Permanent neurological disability Worsening psychosis ```

Answer 49

Disseminated intravascular coagulation (DIC) is an acquired syndrome characterised by activation of coagulation pathways, resulting in formation of intravascular thrombi and depletion of platelets and coagulation factors. Thrombi may lead to vascular obstruction/ischaemia and multi-organ failure. Spontaneous bleeding may occur. Generalised bleeding, evidenced by at least 3 unrelated sites, is highly suggestive of DIC. DIC can be triggered by major trauma, organ destruction, sepsis or severe infection, severe obstetric disorders, some malignancies, major vascular disorders, and severe toxic or immunological reactions. An acquired syndrome characterised by activation of coagulation pathways, resulting in formation of intravascular thrombi and depletion of platelets and coagulation factors. Clinical history can include epistaxis, gingival bleeding, haematuria, oliguria, cough, dyspnoea, fever, delirium, and coma. Physical examination may reveal petechiae, ecchymosis, gangrene, mental disorientation, hypoxia, hypotension, and GI bleeding. Diagnosis is based on presence of ≥1 known underlying conditions causing DIC plus abnormal global coagulation tests: decreased platelet count, increased prothrombin time, elevated fibrin-related maker (D-dimer/fibrin degradation products), and decreased fibrinogen level. Aggressive treatment of the underlying disorder is indicated, as well as fresh frozen plasma, platelet concentrate, antithrombin III, tissue factor pathway inhibitor, heparin, and recombinant factor VII activated for refractory haemorrhagic episodes. Complications include life-threatening haemorrhage, acute renal failure, and gangrene and loss of digits.

Answer 50

Many conditions can cause DIC; therefore, the overall incidence is difficult to determine. Age and sex are not good predictors. Mortality is high. For instance, presence of DIC in patients with major trauma will result in a significant increase in overall mortality. Since the global incidence of many underlying disorders, such as major trauma and sepsis, remains high, decreased incidence of DIC in the near future is unlikely. However, new insights into pathophysiology have led to new treatments that are likely to reduce mortality and morbidity.

Answer 51

``` STRONG Major trauma Burn Organ distraction Sepsis Severe obstetric disorders.complications Solid tumours + Haem malignancies (Release of tissue material and tumour-expressed procoagulants such as tissue factor or cysteine protease into circulation, leading to systemic activation of coagulation) Snake bites, drugs, blood transfusion reactions, and transplant rejection ``` WEAK Major vascular disorders (aortic aneurysms / giant hemangiomas)

Answer 52

COMMON Oliguria, hypotension, tachycardia Purpura fulminans, gangrene or aural cyanosis Delerium or coma Petechiae, ecchymosis, oozing, or haematuria Generalised bleeding, evidenced by at least 3 unrelated sites, is highly suggestive of DIC.

Answer 53

Platelet count - low PT - usually high Fibrinogen - low D-dimer - high APTT - high OR low Imaging studies - Dependent on the underlying disorder and areas of thrombosis and haemorrhage. Can measure clotting factors but usually not necessary

Answer 54

Treat underlying disorder A platelet transfusion should be considered when the platelet count is <20 x 10^9/L (<20 x 10^3/microlitre) or <50 x 10^9/L (<50 x 10^3/microlitre) with active bleeding. Fresh frozen plasma (FFP) is the preferred agent for replacement of coagulation factors and coagulation inhibitors when significant bleeding is present or when fibrinogen levels are <2.94 micromol/L (<100 mg/dL). Cryoprecipitates or fibrinogen concentrates are second-line alternatives. Blood-borne diseases of all types (hepatitis, HIV) and febrile reactions are always a risk in giving human blood products. Rapid infusion of platelets, FFP, cryoprecipitates, or fibrinogen concentrates may cause hypotension. CHRONIC DIC -> needs heparin if coagulation predominant + possible antifibrinolytics -> tranexamic acid

Answer 55

Mortality is high. For instance, presence of DIC in patients with major trauma significantly increases overall mortality. However, new insights into pathophysiology have led to new treatments that are likely to reduce mortality and morbidity. In some cases, such as abruptio placentae, DIC will quickly resolve itself after elimination of the underlying condition.

Answer 56

``` Acute renal failure Life-threatening haemorrhage Cardiac tamponade Haemothorax Intracerebral haematoma Gangrene + loss of digits ```

Answer 57

· GCS < 13 on initial assessment · GCS < 15 at 2 hours after injury on assessment in the emergency department · Suspected open or depressed skull fracture · Any sign of basal skull fracture · Post-traumatic seizure · Focal neurological deficit · More than one episode of vomiting since the head injury Current anticoag treatment AND THEN: · Is there loss of consciousness or amnesia since the head injury? · If so the following RFs justify head CT: · Age > 65 years · A history of bleeding or clotting disorder · Dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from height of > than 1 metre or 5 stairs) · More than 30 minutes’ retrograde amnesia of events immediately before the head injury

Answer 58

An opioid is any synthetic or natural agent that stimulates opioid receptors and produces opium-like effects. Opiates are opioids naturally derived from the opium poppy, Papaver somniferum, and include morphine and codeine. Opioids are used in the treatment of pain but are often sold illicitly and abused for their euphoric effects. An overdose occurs when larger quantities than physically tolerated are taken, resulting in central nervous system and respiratory depression, miosis, and apnoea, which can be fatal if not treated rapidly. The patient's history from bystanders/friends/family can assist diagnosis. Signs include central nervous system and respiratory depression, miosis, and apnoea. Initial treatment consists of ensuring adequate ventilation followed by administration of the opioid antagonist naloxone. Monitor patients for re-sedation and repeat antidote dose if necessary.

Answer 59

During 2016, the rate of synthetic opioid overdose deaths (other than methadone) exceeded those of heroin overdose deaths for the first time in the US (6.2 per 100,000 population vs. 4.9 per 100,000 population, respectively). Recent abstinence, resulting in loss of tolerance (such as during incarceration), increases the risk of overdose. Because of this, drug overdose is the most common cause of death of former inmates after prison release; the risk of death in the 2 weeks after release is 12 times that of the general population.

Answer 60

STRONG Opioid abuse and dependence Recent abstinence in chronic users WEAK Chronic pain

Answer 61

COMMON ``` Miosis Bradypnoea Altered mental status Dramatic naloxone response Fresh needle marks Drug paraphernalia Decreased gastric motility Old track marks on arms/legs ``` UNCOMMON Pulmonary rales Frothy pink sputum Seizures Dysrhythmias - Can be caused by sodium channel blockade with propoxyphene and can be associated with significant respiratory compromise.

Answer 62

1ST Naloxone trial ECG - may be abnormal ECG (e.g., QRS prolongation or signs of myocardial ischaemia) CONSIDER CxR - if suspect ARDS Abdo XR - mule Can do opioid urine screen but usually not necessary

Answer 63

1. Ventilation PRIOR to naloxone administration - Ventilatory support is the most important intervention and may be life-saving on its own. 2. naloxone: (standard syringe) 0.4 to 2 mg intravenously/intramuscularly/subcutaneously, repeat dose every 2-3 minutes, titrate dose by 0.2 to 0.4 mg increments according to response, maximum 10 mg/total dose; (autoinjector) 0.4 mg intramuscularly/subcutaneously initially, may repeat in 2-3 minutes if no response; 2-4 mg into one nostril as a single dose, may repeat in alternate nostrils every 2-3 minutes if necessary according to response; consult specialist for further guidance on dose The endpoint of therapy is the restoration of adequate spontaneous ventilation but not necessarily complete arousal. The duration of naloxone effect is 30 to 90 minutes. Repeat as needed to maintain adequate spontaneous ventilation. IF MULE: whole bowel irrigation

Answer 64

Timely administration of naloxone, and appropriate ventilation prior to antidote, results in complete reversal of the effects of opioid overdose. Provided that patients do not need bolus dosing, the prognosis is excellent. Opioid-tolerant patients who receive larger doses of naloxone and experience withdrawal still have an excellent prognosis, with withdrawal symptoms subsiding in about 1 hour. If the patient suffers significant hypoxia or aspirates gastric contents, complications from these events can result in significant morbidity and mortality.

Answer 65

Hypoxia Aspiration ARDS

Answer 66

opioid overdose Acute respiratory distress syndrome (non-cardiogenic pulmonary oedema) can complicate opioid overdose. This can occur as a result of rapid reversal with naloxone or the effects of the opioid itself. Patients may present with respiratory distress and have rales on auscultation. Some opioids may cause clinical features other than the classical opioid toxidrome after overdose. Propoxyphene can cause sodium channel blockade and lead to wide complex dysrhythmias in overdose. Meperidine, propoxyphene, and tramadol can cause seizures. Dextromethorphan and tramadol may cause features of serotonin toxicity. Opiates are sometimes illegally imported by 'body packing'. Sealed drug-filled packets are designed to be swallowed and defecated at the destination. If a packet ruptures, large amounts of pure undiluted (uncut) opiate, often heroin, are released, requiring large amounts of naloxone. 'Body packers' or 'mules' are at risk of delayed or prolonged poisoning as a result of package rupture.

Answer 67

The recommended dose of paracetamol is 4 g (or 75 mg/kg) in 24 hours for an adult patient. Any ingestion exceeding this is regarded as an overdose. However, toxicity is extremely unlikely if <75 mg/kg paracetamol has been ingested within a 24-hour period. Patients are often asymptomatic or have only mild gastrointestinal symptoms at initial presentation. Untreated paracetamol poisoning may cause varying degrees of liver injury over the 2 to 4 days following ingestion, including fulminant hepatic failure. Rarely, massive overdose may initially present with coma and severe metabolic acidosis. Presentation with coma may also occur if a combination preparation of paracetamol and opioid is taken in overdose, or after an overdose of multiple drugs. Hepatotoxicity is extremely rare in patients treated with acetylcysteine within 8 hours of an acute paracetamol overdose. The efficacy of acetylcysteine decreases subsequent to the first 8 hours following an acute paracetamol overdose, with a corresponding stepwise increase in hepatotoxicity with increasing treatment delays between 8 and 16 hours.

Answer 68

Paracetamol is one of the most frequently used drugs in intentional overdoses. In the UK, paracetamol is the most common drug taken in overdose, accounting for 48% of poisoning admissions to hospital and associated with an estimated 100 to 200 deaths per year.

Answer 69

STRONG Hx self-harm Hx of repeated painkiller use Glutathione deficiency Cyp450 inducers - Long-term treatment with cytochrome P450 2E1 inducers (e.g., phenobarbital, isoniazid) or long-standing alcohol abuse may increase the risk of liver damage following paracetamol overdose.

Answer 70

``` COMMON Attempted self harm Hx of repeated painkiller use Asymptomatic at presentation NV + abdo pain ``` UNCOMMON RUQ pain + tenderness Jaundice Confusion, dec consciousness level +/or asterixis

Answer 71

Serum paracetamol Serum AST + ALT - may be elevated ABG - ph + lactate - may show acidaemia; lactate level may be elevated Urea + electrolytes - may show renal impairment PT + INR - PT may be prolonged; INR may be increased Consider Urine drug screen Serum salicylate level

Answer 72

<8 HOURS SINCE INGESTION Acetylcysteine - acetylcysteine: children and adults: 150 mg/kg intravenous infusion over 1 hour, followed by 50 mg/kg infusion over 4 hours, then 100 mg/kg infusion over 16 hours Supportive - May include physiological support such as intubation and ventilation or vasoactive infusions for blood pressure support, psychological support for mental illness, and education for those with accidental overdoses. Ondansetron IV anti-emetic Activated charcoal IF within 2 hours of ingestion Referral for liver transplant is indicated if: arterial lactate concentration >3.5 mmol/L after fluid resuscitation; OR arterial pH <7.3, and lactate >3.0 mmol/L after fluid resuscitation; OR PT/INR >100 seconds/6.0 seconds AND encephalopathy grade 3 or more AND creatinine >292 micromol/L (3.3 mg/dL) within 24 hours AND a normal arterial pH.

Answer 73

Oral Acetylcysteine-related N+V IV acetylcysteine-related coagulopathy IV acetylcysteine-related anaphylaxis Acute liver failure

Answer 74

In survivors, hepatic regeneration is normally rapid and complete, with normalisation of liver function tests within 1 to 3 weeks. Renal injury is rare, and when it occurs serum creatinine typically begins to rise soon after serum aminotransferase activity has peaked. Occasionally, renal injury occurs without liver injury. In unselected patients referred to hospital without specific therapy, <10% developed hepatotoxicity; 1% developed acute renal failure; and 1% to 2% died in hepatic failure.

Answer 75

Acute liver injury or fulminant hepatic failure of undetermined aetiology may occur if a paracetamol overdose has been taken several days earlier. Coma and severe metabolic acidosis may precede the development of hepatotoxicity in acute massive paracetamol overdose (serum concentration >5290 micromol/L [800 micrograms/mL]). Coma and respiratory depression may occur if a combination preparation of paracetamol and opioid has been ingested.

Answer 76

Acute cervical spine trauma encompasses a wide range of potential injuries to ligaments, muscles, bones, and spinal cord that follow acute incidents ranging from a seemingly innocuous fall to a high-energy motor vehicle accident. Patients may present immediately after a traumatic incident or days to weeks later. In all cases, careful investigation is required to ensure that the stability of the cervical spine has not been compromised, because, in extreme cases, cervical spine instability can lead to progressive neurological deficit, quadriplegia, and even death. Mechanism of injury is highly variable, ranging from seemingly innocuous falls to high-energy motor vehicle accidents. Possible presentations include neck pain, limited range of motion, and/or neurological deficit. A high index of suspicion and proper investigation is required to detect bone or ligament damage that can otherwise result in spinal cord injury. If suspected, immediate cervical spine stabilisation is essential until serious injury can be excluded by neurological assessment and CT scan or other imaging. Maintenance of mean arterial blood pressure and consideration of the use of methylprednisolone are potentially important and time-sensitive therapeutic interventions. The use of methylprednisolone, while certainly time-sensitive, is an intervention whose efficacy is debated among professionals. Early consultation with a specialist is advisable to avoid delays that may affect patient outcome.

Answer 77

The incidence of crash-related neck injury varies widely among European countries, with the highest rates reported in the UK and the lowest rates in France and Finland. The majority of studies showed a high male-to-female ratio and an age of peak incidence of younger than 30 years old. Traffic accidents were typically the most common cause of spinal cord injury, followed by falls in the elderly population

Answer 78

STRONG ``` Male Female (whiplash) Lack of preparation or awareness of collision Head rotation at time of collision Previous Cspine trauma or surgery ``` WEAK Pre-existing spinal, cranial, or other abnormality

Answer 79

``` COMMON Male 18-25 Intoxication Numbness/tingling or weakness Bowel/bladder dysfunction Motor weakness Sensory loss ``` ``` UNCOMMON Reduced/painful range cervical motion Loss of anorectal tone SPASTICITY ONLY DEVELOPS WEEKS LATER Hyperreflxia Babinski Hoffman Neurogenic shock Spinal shock Resp-change CN deficit - Injury at the occipital-cervical junction may lead to lower brainstem or cranial nerve injury. ```

Answer 80

Axial CT cervical spine with 3D reconstructions MRI cervical spine - more sensitive for the identification of soft-tissue injuries than CT and is considered the reference standard in identifying injuries to the spinal cord and soft tissues Consider Nerve conduction studies - Ordered if radiculopathy is suspected. Slowing of nerve conduction occurs with peripheral nerve compression.

Answer 81

Immobilisation Emergency neurosurgical referral if high probability of neurological injury Methylprednisolone sodium succinate: 30 mg/kg intravenously as a loading dose, followed by 5.4 mg/kg/hour intravenous infusion for 23 hours - WITHIN 8 HRS OF INJURY Patients with fractures and central cord syndrome (CCS) should be definitively treated through internal and/or external immobilisation in consultation with a surgical service. In those without fractures and CCS, it is safe and reasonable to consider early surgery for profound neurological dysfunction (ASIA grade C) and ongoing compression due to developmental cervical canal stenosis.

Answer 82

acute cervical spine trauma The majority of patients present immediately following some form of trauma such as a fall, motor vehicle accident, or sporting injury (particularly rugby, American football, trampolining, or diving into swimming pools). Potentially less obvious presentations include stroke victims who may have had an associated fall and a cervical spine injury that has gone undetected; this should be considered especially when a stroke victim has bilateral signs and symptoms. Similarly, intoxicated patients for whom the history is vague may have head injuries that are consistent with potential cervical spine trauma. Although most patients present at the time of injury, there are reports of patients with significant cervical spine injuries presenting many days or weeks after injury, and the clinician must be vigilant for this possibility.

Answer 83

Most patients with uncomplicated neck pain will recover completely in a matter of days to weeks. A minority (as many as 25% or 30%) will experience persistent symptoms, often in the absence of readily observed pathology (such as disc herniation). Patients with a prior whiplash injury have been found to have a poorer prognosis after a second injury.

Answer 84

``` Vertebral artery dissection Permanent neuro disability Death Chronic pain syndromes Chronic headache Prolonged symptoms post mild traumatic brain injury (>3m) Upper extremity radiculopathy Myelopathy with cervical disc herniation Cervical facet pain Cervical mechanical pain Post-Injury medication dependence ```

Answer 85

Tendinopathy is a general term that describes tendon degeneration characterised by a combination of pain, swelling, and impaired performance. Common sites include the rotator cuff (supraspinatus tendon), wrist extensors (lateral epicondyle) and pronators (medial epicondyle), patellar and quadriceps tendons, and Achilles' tendon. The exact aetiology is unclear. Studies suggest it is an over-use condition leading to inadequate tendon repair that predisposes the tendon to micro-tears and degeneration. Treatment consists of activity modification, relative rest, ice, stretching, and strengthening. Stretching and strengthening are best guided by a physiotherapist. Extracorporeal shockwave therapy or ultrasound-guided injection of platelet-rich plasma may be considered in recalcitrant tendinopathy, but their use remains controversial. Those who do not improve with conservative therapy should seek surgical evaluation. There are over 600 muscle-tendon units in the human body. Theoretically, tendinopathy can occur in any one of them. However, this monograph will focus on the common sites including: the rotator cuff (supraspinatus tendon) in the shoulder, wrist extensors (lateral epicondyle) and pronators (medial epicondylitis) in the elbow, patellar and quadriceps tendon in the knee, and Achilles' tendon in the heel. In athletes, common locations for tendinopathy include the Achilles' and patella tendons. In the general population, the Achilles' and lateral epicondyle are the most commonly affected. There are many terms used to characterise chronic tendon disorders. Tendonitis refers to a painful tendon with histological signs of inflammation within the tendon. Tendinosis is a localised intrinsic degeneration of unknown aetiology, characterised by localised swollen tendon nodes. Several studies have shown that tendon biopsies taken at surgery lack inflammatory cells.[1][2][3] In clinical settings, tendinopathy describes impaired tendon healing characterised by pain, swelling, and impaired performance.

Answer 86

Because tendinopathy affects such a diverse population and can occur at different sites, the true incidence is unknown. However, it is estimated that half of all sports injuries are secondary to over-use. Of these injuries, the muscle-tendon unit is the most commonly affected. Approximately 10% of runners develop Achilles' tendinopathy, which tends to affect men aged >30 years. Patellar tendinopathy usually affects young adults in their teens to 30s, but can also occur in older individuals. There is a 1% to 3% annual incidence of lateral epicondylitis, which affects men and women equally. It is more common in people aged >40 years.

Answer 87

Tendons serve several functions including mechanical force transmission, joint stabilisation, and shock absorption to limit muscle damage. Tendons consist of collagens, proteoglycans, glycoproteins, water, and cells. They are able to alter their structure and composition in response to mechanical loads. While appropriate mechanical loading of tendons is beneficial, over-use (chronic, repetitive mechanical loading placed on tendons) results in pathological changes

Answer 88

STRONG Athlete Unsuitable equipment Hard + high friction playing surface WEAK Increasing age Fluoroquinolone Rx

Answer 89

``` COMMON RFs Insidious onset Well-localised tenderness Pain during activity ``` UNCOMMON Tendon thickening Tendon nodularity Crepitis TESTS: Test for medial epicondylitis: resisted forearm pronation and palmar flexion elicits pain at the medial epicondyle Test for lateral epicondylitis: resisted wrist extension with elbow in full extension stresses the origin of the extensor carpi radialis brevis tendon and elicits pain at the lateral epicondyle Medial and lateral pressure applied anterior and superior to the Achilles' insertion elicits pain Impingement test: with shoulder in 90º forward flexion, elbow in 90º flexion, apply downward pressure on the hand while stabilising at the elbow. Pain = positive test

Answer 90

Clinical Diagnosis Ix to consider US - thickened, blurred tendon, and possible hypoechoic foci within tendon MRI - thickened tendon with intermediate signal intensity (grey/white)

Answer 91

CONSERVATIVE: Main treatment is rest, plus evaluating and correcting over-training errors. Physiotherapy starts with stretching to improve range of motion followed by strengthening of the rotator cuff muscles and scapular stabilisers 2 or 3 times per week for 6 weeks. May need multiple courses. Exercise, incorporating loaded exercise (i.e., against gravity or resistance), has been found to be effective in the treatment of rotator cuff tendinopathy with respect to pain and functional disability. Physiotherapy modalities - PHONOPHORESIS (US delivered medicine) and iontophoresis (Electric current delivered) ICE ``` MEDICAL NSAIDs: EG Ibuprofen 400-600mg orally 4-6hrly Naproxen 500mg orally BD ``` Corticosteroid injections (can allow physio) ONCER PER 3m GTN PATCH - Glyceryl trinitrate patches are thought to decrease pain, specifically chronic pain, by improving tendon healing SURGERY CAN OFFER PLATELET RICH PLASMA THERAPY ``` MISCELLANEOUS Extracorporeal shockwave therapy Low-level laser therapy Counterforce brace (eg lateral epicondylitis) Patellar braces Heal lifts for achilles tendinopathy ```

Answer 92

In general, the majority of patients should improve with conservative measures.

Answer 93

Tendon rupture low risk

Answer 94

Tendinopathy

Answer 95

Tendinopathy

Answer 96

A torn anterior cruciate ligament (ACL) usually occurs as the result of an acute non-contact deceleration injury, forceful hyperextension, or excessive rotational forces about the knee. The ligament may be completely torn, partially torn, or avulsed from its origin or insertion. The ACL is the primary restraint to excessive anterior translation and rotation of the tibia on the femur; therefore, complete ACL disruption typically results in dynamic knee instability or the inability to respond to quick changes in position. Injury typified by sudden, painful, audible pop noise. Patient typically presents with inability to return to activity, joint instability, and rapid development of effusion (haemarthrosis). Often tender at lateral femoral condyle, lateral tibial plateau, and tibiofemoral joint lines. A positive Lachman's test is most accurate right after the injury and the pivot shift test is more useful in sub-acute or chronic cases. History and physical examination usually provide accurate diagnosis. X-rays obtained to rule out avulsion fractures or other related conditions, but do not directly identify ACL injury. MRI delineates ACL tears nicely, along with associated injury to menisci and other structures. Initial treatment for most patients consists of protection, rest, ice, compression, elevation, and analgesia (as appropriate). Subsequent treatment varies by an individual patient's health and fitness status and goals. Treatment may range from minimal or no additional intervention to bracing, physiotherapy, and activity modification, and to surgical reconstruction (either early or delayed).

Answer 97

The 15- to 45-year-old age group is at highest risk. Injuries occur primarily among active people, especially in sport involving cutting, pivoting, and decelerating (e.g., soccer, basketball, skiing) or contact (e.g., rugby). About 70% of ACL tears occur during sport activities. In children, falling off of a bike while trying to plant the ipsilateral foot is a common mechanism of ACL avulsion from the tibial eminence. The estimated US incidence is 100,000 to 200,000 ACL tears per year, with 100,000 ACL reconstructions per year. The female-to-male ratio has generally ranged from 2:1 to 8:1, and varies across sports. Non- or minimal-contact injuries account for majority of ACL injuries (up to 70%), especially in females.

Answer 98

``` STRONG Acute trauma Female sex Poor technique for landings Hx Studs or spikes use Rough or uneven playing surface Ground condition/weather Fatigue Increased risk in adolescents and young adults, but middle-aged athletes/skiers also involved. Skeletally immature athletes more likely than adults to avulse ACL insertion rather than have intra-substance tear. ``` WEAK Athletes who play more aggressively have a higher propensity for injury.

Answer 99

``` COMMON Audible pop Rapid knee swelling Inability to return to activity Sensation of knee instability/buckling Pain +ve Lachmans +ve pivot shift +ve anterior drawer test Tenderness at femoral condyle, lateral tibial plateau ```

Answer 100

Xray - impaction fracture of the lateral femoral condyle and fracture of the posterior aspect of the lateral tibial plateau (uncommon); radiographic drawer sign (anterior subluxation of tibia on femur) (uncommon); effusion (common); bony avulsion of ACL at intercondylar tubercle (mainly in skeletally immature patients) Ottawa knee rules recommend x-rays in acute knee injury in an adult if any of the following features is present: Inability to bear weight at time of injury and at time of evaluation Isolated tenderness at patella or fibular head Active flexion of knee <90 degrees Age >55. MRI - ACL fibres appear disrupted, blurry on T1 sequences, with abnormal high signal on T2 images

Answer 101

``` Conservative: PRICEM Protected Weight baring Rest Ice Compression Elevation Bracing ``` Medical: NSAIDS Surgical: - bone-patellar tendon-bone autograft (intra-articular technique) - hamstring tendon grafts (various bundling/augmentation and tunnelling approaches - intra-articular technique) - cadaveric allograft (intra-articular technique)

Answer 102

However, with surgical reconstruction and proper physiotherapy, 41% to 92% of athletes are able to return to their pre-injury level of activity. Non-operative outcomes seem to be worse in skeletally immature and more active patients. However, for those who are able to rehabilitate well, make certain lifestyle modifications, and psychologically cope with their limitations, a non-operative approach can yield good outcomes. Over time, it has been shown that up to 60% or more of people who have had an ACL tear will develop post-traumatic knee arthrosis.

Answer 103

``` Bone bruising MCL injury Post-traumatic arthritis Meniscal tear Articular Cartilage Injury ```

Answer 104

ACL tears may also occur after slips and falls, twisting injuries to the knee, and high-energy injuries (e.g., motor vehicle accidents). The ACL may be injured alone (isolated) or as part of a more complex injury (multiple ligamentous injuries, meniscal tear, knee dislocation). Complete, intrasubstance tears of the ligament are the most commonly seen injury. Many partial tears involve enough fibres to cause significant instability.[4][5] ACL bony avulsion (tibial eminence) injuries mainly occur in skeletally immature individuals.[6][7] In children, falling off of a bike while trying to plant the ipsilateral foot is a common mechanism of ACL avulsion from the tibial eminence.[8]

Answer 105

An antidepressant overdose occurs when a person ingests an amount of medication that is more than a reasonable and normal dose. Tricyclic antidepressants (TCAs) are the main cause of damaging antidepressant overdose because, unlike other antidepressants, they have a narrow therapeutic range and become potent cardiovascular and central nervous system toxins in moderate doses. Tricyclic antidepressants have a narrow therapeutic index and therefore become potent cardiovascular and central nervous system toxins in moderate doses. Complications include effects of prolonged hypotension, cardiac arrhythmias, and seizure. Death results from cardiovascular collapse. Best markers for suspected overdose are a history of depression, suicidality, and overdose with a sudden deterioration in mental status and vital signs. At 1 to 2 hours after ingestion, there is a rapid decline in mental and cardiovascular status. Diagnosis is established on clinical grounds and classic ECG changes (sinus tachycardia progressing to wide complex tachycardia and ventricular arrhythmias with increasing severity of intoxication). Hypertonic sodium bicarbonate improves conduction abnormalities and hypotension. Management of arrhythmias involves correction of acidosis, hypoxia, and electrolyte imbalance. Anti-arrhythmic drugs should generally be avoided. Hypotension usually responds to correction of hypoxia and administration of intravenous fluids and sodium bicarbonate. Treatment with vasopressors (such as norepinephrine [noradrenaline]) is controversial and should only be done in consultation with a medical toxicologist or intensive care specialist . Benzodiazepines are the first-line treatment for seizures.

Answer 106

A UK cohort study found that TCAs and tetracyclic antidepressants (ICD-10 code T43.0) were the tenth most common poisoning substance, accounting for 624

Answer 107

``` STRONG Hx depression OCD Chronic Pain Attention deficit hyperactivity disorders ```

Answer 108

Change in mental status Tachycardia Hypotension Mydriasis (part of the anticholinergic toxidrome) Warm, dry, flushed skin Decreased or absent bowel sounds Urinary retention Ophthalmic signs - Divergent squint, internuclear ophthalmoplegic and gaze paralysis; nystagmus may also be seen. Neurological signs - Ataxia, and myoclonic and choreoathetoid movements, may be seen. Increased muscle tone, hyperreflexia, and extensor plantar responses may occur.

Answer 109

ECG - tachycardia; QRS prolongation >100 milliseconds; terminal 40 milliseconds rightward axis deviatio Sodium bicarb therapeutic trial - narrowing of QRS ABG - metabolic acidosis Serum TCA concentrations Possibly check: paracetamol/salicylate Urine drug screen

Answer 110

The patient should be rapidly stabilised. Assess airway, breathing, and circulation; obtain intravenous access; attach a cardiac monitor; and obtain an ECG to look for QRS prolongation. Acidosis, hypoxia, and electrolyte abnormalities should be corrected initially. Ingestion within 2 hours: activated charcoal: 1 g/kg orally as a single dose, repeat every 2-4 hours if required With QRS >100 milliseconds or pH <7.45: Sodium bicarbonate: 1-2 mEq/kg intravenously Hypotension: IV fluid bolus +/- vasopressors or glucagon pr ECMO Seizure - terminate with benzo/barbs/propofol

Answer 111

Outcome depends on the degree of overdose as well as the comorbidities of the patient. Death occurs either from early cardiac arrest or from late refractory hypotension. Young, healthy people with mild-to-moderate overdoses tend to do extremely well when therapy is aggressive. Mortality in healthy people with large overdoses is also typically low if correctly managed, although some patients may succumb to their overdose despite appropriate therapy. Older people, and those with comorbidities affecting their cardiovascular status, often have higher morbidity and mortality even with a moderate overdose. Patients who show no significant signs of TCA overdose for at least 6 hours after arrival are expected to do well.

Answer 112

``` Arrhythmias Delerium Sezure Coma Cardiac arrest ```

Answer 113

Some chronically poisoned patients retain their mental status, exhibit stable vital signs, and complain only of fatigue. These patients may also exhibit a history of falls or hip fractures. These symptoms are caused by development of orthostatic hypotension as a result of the alpha-1 antagonism caused by TCAs, leaving older patients most susceptible. Also, after an acute overdose the vital signs and ECG findings may resolve and the patient is left with a residual anticholinergic delirium. This is typically manifested by garbled speech and disorientation with visual and/or tactile hallucinations.

Answer 114

Some chronically poisoned patients retain their mental status, exhibit stable vital signs, and complain only of fatigue. These patients may also exhibit a history of falls or hip fractures. These symptoms are caused by development of orthostatic hypotension as a result of the alpha-1 antagonism caused by TCAs, leaving older patients most susceptible. Also, after an acute overdose the vital signs and ECG findings may resolve and the patient is left with a residual anticholinergic delirium. This is typically manifested by garbled speech and disorientation with visual and/or tactile hallucinations.

Answer 115

Benzodiazepine (BZD) overdose occurs when excessive amounts of BZD medications are taken. Acute overdose is characterised by excessive sedation with impaired mental status and diminished postural stability and reflexes. Diagnosis is suggested by the history and by exclusion of other aetiologies. Chronic overuse increases the risk of many other pathologies. Benzodiazepines (BZDs) are the most commonly prescribed medications for anxiety, sedation, and sleep. Overdose can be intentional in suicidal patients; accidental in combination with other central nervous system (CNS) depressants, such as alcohol and opioids, and in older people; and occasionally by medication error. Older people, who commonly have diminished drug clearance and polypharmacy, are at especially high risk of overdose. The key feature is excessive sedation with unremarkable vital signs and anterograde amnesia. Larger doses can cause coma and respiratory depression. Treatment of overdose is by symptom management, not by quantitative assay. Acute management consists of maintaining airway, respiration, and haemodynamic support while excluding other diagnoses. Assisted ventilation may be necessary. Death is uncommon. Most deaths from BZD overdose are from respiratory depression as a result of mixed overdoses with BZD and other respiratory depressants, particularly alcohol and opioids. The BZD antagonist flumazenil can be used in first-time or infrequent BZD users to reverse CNS depression. It is contraindicated in BZD-dependent patients because of the risk of provoking seizures. The risks associated with its use often outweigh the benefits.

Answer 116

BZD use is higher in white people than in other ethnic groups. Twice as many females as males use BZDs. Sedatives, anxiolytics, and hypnotics are commonly prescribed for people in the sixth and seventh decades of life. Prevalence of BZD use has been reported as ranging from 3.9% in middle-aged and older adults in Brazil, to 35.9% in people aged 65 years and older in Canada. Non-medical use of BZDs is highest in people aged 18 to 25 years, with rates of 0.7% to 1.9%.

Answer 117

STRONG ``` Depression Hx illicit drug/Alcohol Drug administration error Comorbidity Hx of BZD use Hx of polydrug ingestion Suicidal ideation/behaviour Older age ``` WEAK Drug interaction Biogenetic susceptibility

Answer 118

COMMON Impaired mental status Drowsiness, slurred speech, ataxia Decreased deep tendon reflexes ``` UNCOMMON Coma Resp depression Nystagmus Paradoxical stimulation ```

Answer 119

Pulse Ox FBC - normal Serum chemistry with BG Serum ethanol Urine toxicology screen - negative result with pure BZD overdose; positive result indicates co-ingestion of other drugs or illicit substances ECG Flumenazil trial - resolution of symptoms confirms BZD overdose

Answer 120

Management of pure benzodiazepine (BZD) overdose is supportive, consisting of airway maintenance, cardiorespiratory monitoring and support, and intravenous fluids. Mixed overdose and other causes of central nervous system depression should be ruled out. Flumazenil: 0.2 mg intravenously given over 30 seconds; may give a further 0.3 mg after 30 seconds if necessary; further doses of 0.5 mg may be given at 1 minute intervals as necessary, maximum 2 mg total dose

Answer 121

Most patients make a full physical recovery after acute benzodiazepine overdose but, in many cases, the underlying psychiatric and social issues that precipitated the overdose need to be addressed. Patients who have taken an intentional overdose are at risk of future episodes of deliberate self-harm.

Answer 122

Respiratory arrest | Coma

Answer 123

Patients with benzodiazepine (BZD) overdose may present to the ED in an obtunded state. There may be little or no history, and he or she may otherwise be known to be a healthy person. If brought in by a friend or relative, vague information may be gathered about the emotional state of the patient or the discovery of empty pill bottles. Medications with similar-sounding names to BZDs - for example, clozapine (an atypical antipsychotic) and clonazepam - can be confused, with potential for severe overdose attributable to significant differences in the daily dose between the two drugs. Another presentation may result from administration of flunitrazepam, a potent BZD often surreptitiously given to victims for the purpose of robbery or rape. It is favoured by perpetrators not only because it is a rapidly acting and powerful sedative, which can easily be disguised in a drink, but also because it is a powerful amnestic, making accusations and prosecution difficult. Flunitrazepam is prohibited in the US as a Schedule I Controlled Substance, but is widely marketed in some countries by Roche under the trade name Rohypnol. It is also a popular recreational drug, with street names such as Roofies, Roach, and Mexican Valium.[2] The patient may present to the ED indicating he or she was drugged, and had visited a bar alone the previous night. The patient may also note having no memory of the evening and may notice money stolen, or signs of physical or sexual attack.

Answer 124

Digoxin is the most commonly prescribed cardioactive corticosteroid in the US. In therapeutic doses, they increase cardiac contractility and control the heart rate. Digoxin toxicity is a clinical diagnosis that relies in part on ECG findings such as signs of increased automaticity and AV node blockade (PVCs, slowed ventricular response). Serum digoxin concentration (SDC) is usually greater than the therapeutic range of 0.6 to 1.2 nanomol/L (0.5 to 0.9 nanograms/mL), but may not be elevated. Can be acute or chronic, intentional, or accidental. Typically presents with components of GI, constitutional, and/or cardiovascular symptoms. Diagnosis is based on symptoms and laboratory data. At therapeutic digoxin doses (0.6-1.2 nanomol/L [0.5 to 0.9 nanograms/mL]), the ECG typically shows PR-interval prolongation and a scooped ST segment. In overdose, ECG also shows signs of increased automaticity (PVCs), AV nodal blockade, and slowed ventricular response. Treatment includes digoxin-specific antibody fragments and supportive care. Lidocaine and phenytoin can be used for cardiac dysrhythmias when antibody fragments are unavailable. There are no long-term complications of poisoning in patients treated appropriately for chronic digoxin toxicity, as long as anoxic brain injury, myocardial infarction, or terminal dysrhythmias have not occurred prior to treatment.

Answer 125

Patients aged >55 years are more commonly affected, but toxicity occurs in both young and old people.

Answer 126

``` STRONG Age >55 Decreased renal clearance Hyperkalaemia Hypokalaemia Concomitant use of specific drugs: ``` Digoxin is largely dependent on p-glycoprotein for elimination. Thus, medications that inhibit p-glycoprotein may increase digoxin levels and potentially cause toxicity. These are numerous, but clinically significant ones include verapamil, diltiazem, amiodarone, quinidine, ketoconazole, itraconazole, vinblastine, doxorubicin, 2,4-dinitrophenol, and erythromycin.[18] Others include clarithromycin, ciclosporin, propafenone, quinidine, and spironolactone. Hypomagnesaemia Hypercalcaemia WEAK Hypothyroidism

Answer 127

COMMON Digoxin exposure GI symptoms - Typically include nausea, vomiting, diarrhoea, abdominal pain, or anorexia. CNS symptoms - Typically include lethargy, weakness, and confusion. Xanthopsia Suicidality CV Sx - Typically include palpitations, syncope, arrhythmias, and dyspnoea.

Answer 128

ECG - PVCs, bidirectional ventricular tachycardia, atrial tachycardia with variable or slow ventricular response, accelerated junctional rhythms Serum digoxin concentration - over the therapeutic range of 0.6 to 1.2 nanomol/L (0.5 to 0.9 nanograms/mL) Serum potassium - hyperkalaemia (>5.0 millimol/L [>5.0 mEq/L]) or hypokalaemia (<3.0 to 3.5 millimol/L [<3.0 to 3.5 mEq/L]) Serum magnesium - may be low Serum creatinine + urea - may be elevated

Answer 129

Activated charcoal: 1 g/kg orally as a single dose, repeat every 2-4 hours if required, maximum 4 doses total General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities. Patients with hypokalaemia or hypomagnesaemia require additional potassium or magnesium with careful monitoring to restore normal serum levels. IF SEVERE - digoxin immune Fab: consult specialist for guidance on dose With symptomatic bradycardia/high-degree AV block: atropine: children: 0.02 mg/kg (minimum 0.1 mg, maximum 0.5 mg) intravenously as a single dose, may repeat once only, maximum 1 mg/total dose; adults: 0.5 mg intravenously every 3-5 minutes, maximum 3 mg/total dose With ventricular tachyarrhythmias: phenytoin: children: 1.25 mg/kg intravenously every 5 minutes, maximum 15 mg/kg total dose; adults: 50-100 mg intravenously every 10-15 minutes, maximum 15 mg/kg total dose lidocaine: children: 1 mg/kg intravenous bolus initially, followed by 30-50 micrograms/kg/min infusion; adults: 1 to 1.5 mg/kg intravenous bolus initially, followed by 1-4 mg/min infusion Ideally, digoxin is discontinued and a different medicine for rate control or a different inotrope prescribed (for AF, atrial flutter or CHF, respectively).

Answer 130

Patients who present with acute digoxin toxicity and have serum potassium concentrations of ≥5.0 millimol/L (≥5.0 mEq/L), who remain untreated and/or undiagnosed, have a mortality of 50%. Patients who present with chronic digoxin toxicity and remain undiagnosed and/or untreated have a reported mortality of 5% to 13%. The prognosis for patients who are treated appropriately is very good. Patients generally have no long-term adverse outcomes related to their toxicity from digoxin.

Answer 131

Anaphylaxis for digoxin Fab Recurrence of AF or HF after digoxin Fab Cardiac Arrest

Answer 132

digoxin overdose

Answer 133

digoxin overdose

Answer 134

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to an infection. Septic shock has also been redefined as a subset of sepsis, in which there is co-existence of: persistent hypotension requiring vasopressors to maintain mean arterial pressure ≥65 mmHg; and serum lactate >2 mmol/L (>18 mg/dL). Findings are generally non-specific and secondary to primary infection. They include malaise, leukocytosis, tachypnoea, and pulse >90 bpm. Sepsis can progress rapidly to multi-organ failure and shock, and is often fatal. Survival is dependent on a high index of suspicion of sepsis, early recognition and immediate intervention. Patients with evidence of sepsis, including signs of organ dysfunction, require immediate hospital assessment. Empirical broad-spectrum antibiotic therapy (based on the most probable pathogens) should be administered as soon as possible, and always within the first hour following recognition. Blood cultures, as well as cultures of all wounds or other potentially infected body fluids, should be performed as indicated by symptoms and the risk profile of the patient, ideally before the initiation of antimicrobial treatment. Any source of infection should be controlled as a matter of urgency, preferably within 6 hours following recognition. Evidence of hypoperfusion or shock should be identified and treated with immediate intravenous fluid challenges, if present. Shock that fails to respond to fluid challenges necessitates urgent critical care referral for consideration of vasopressors and/or inotropes.

Answer 135

Sepsis is estimated to affect 31.5 million people worldwide every year, with an estimated 5.3 million deaths annually. The annual incidence of sepsis in the EU has been estimated at 90.4 cases per 100,000 population. Most epidemiological studies find sepsis to be more common in men than in women. Patients above 65 years old are particularly susceptible, with one study finding almost two-thirds of cases to be in this age group.

Answer 136

STRONG ``` Underlying malignancy Age >65 Immunocompromise Haemodialysis Alcoholism DM Recent surgery Breached skin integrity Indwelling lines or catheters IVDU Pregnancy ``` ``` WEAK Urban residence Lung disease Male Non-white Winter season ```

Answer 137

COMMON ``` High/low temp Tachycardia Tachypnoea Acute altered mental status Poor cap refill, mottling, ashen appearance Signs associated with source of infection Low O2 saturation Arterial hypotension Decreased urine output Cyanosis Purpura fulminans - sign of organ dysfunction. Jaundice Ileus ```

Answer 138

SEPSIS 6 3 out: blood culture, UO, ABG (lactate) 3 in: O2, empirical ABx, IV fluids FBC - WCC high/low Blood urea + electrolytes - serum electrolytes frequently deranged; blood urea may be elevated Serum creatinine - may be elevated LFTs - elevated bilirubin, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and gamma glutamyl transpeptidase Coag studies - deranged Serum glucose - may be elevated or, more rarely, low Lactate levels - may be elevated; levels >2 mmol/L (>18 mg/dL) associated with adverse prognosis; even worse prognosis with levels >4 mmol/L (>36 mg/dL) CRP - elevated Blood culture - may be positive for organism Other source cultures CXR ECG ABG - PaCO₂ <4.3 kPa (32 mmHg) is one of the diagnostic criteria for systemic inflammatory response syndrome; may be hypoxaemia, hypercapnia Consider LP Echocardiogram CT chest/abdo - may show evidence of infection, such as consolidation or pleural effusion, cardiac abnormalities, or a pneumothorax

Answer 139

``` ABx broad spectrum Fluid Resus General intensive care measures include stress ulcer prophylaxis with histamine H2 receptor antagonists or proton pump inhibitors (in patients at risk of gastrointestinal bleeding), deep venous thrombosis prophylaxis (with heparin and compression stockings), enteral or parenteral nutrition, and glycaemic control. Vasopressors Inotrope - dobutamine ```

Answer 140

The mortality rate from sepsis has been estimated in a number of studies to be between 28% and 50%. Intensive care setting (ICU)-specific mortality has been shown to be 27% to 32% in patients with sepsis, and 50% to 70% in patients with septic shock, compared with 14% in ICU patients without sepsis.

Answer 141

``` Renal dysfunction Hypotension ARDS Myocardial dysfunction + failure Multiple organ system failure Hepatic encephalopathy DIC Neurological sequelae Death ```

Answer 142

Sepsis may complicate benign primary infections found in any age group and requires a high suspicion for the clinical signs of systemic inflammatory response (tachycardia, fever, tachypnoea, or respiratory compromise). Altered mental status may also be a presenting feature, especially in older patients. Mild disorientation or confusion is common with more severe presentations, including significant anxiety, agitation, and loss of consciousness. Other features that may be present include reduced urine output; a mottled or ashen appearance; cyanosis of skin, lips, or tongue; or presence of a non-blanching rash on the skin.

Answer 143

Compartment syndrome is a pathological condition characterised by elevated interstitial pressure in a closed osteofascial compartment that results in microvascular compromise (restriction of capillary blood flow). The compartments most commonly involved are those with relatively non-compliant osseous or fascial structures, such as the anterior and deep posterior compartments of the leg and the volar compartment of the forearm. Significant muscle damage can occur with compartment pressures >30 to 40 mmHg or within 10 to 30 mmHg of diastolic BP. Results from increased interstitial pressure in closed osteofascial compartments. Can be caused by fracture, compartment haemorrhage, direct soft-tissue injury, or direct muscular injury. High index of suspicion and early recognition are crucial. Intracompartmental pressures >30 to 40 mmHg or within 10 to 30 mmHg of diastolic BP are associated with significant muscle damage. Palpable pulses distal to the involved compartment do not rule out compartment syndrome. Prompt decompression by fasciotomy is mandatory to prevent muscle ischaemia and rhabdomyolysis.

Answer 144

Compartment syndrome is associated with a diverse range of conditions and it is not possible to state specific epidemiological characteristics.

Answer 145

STRONG ``` Trauma Bleeding disorders Compression support Thermal injury Intense muscular activity ``` WEAK Extravasation of IV infusion Venous obstruction

Answer 146

``` Pain Pressure Paraethesia Pulseless (late sign) Pallor Paralysis ``` Furthermore, pain disproportionate to the severity of injury in an at-risk patient is an important sign that should not be missed.

Answer 147

Compartment pressure measurement - variable; differential pressure within 20-30 mmHg of the diastolic pressure (delta pressure) is considered a strong indicator for fasciotomy Serum CK - elevated Urine myoglobin - elevated

Answer 148

REMOVE any dressing/casts Analgesia - morphine Fasciotomy - If symptoms are not relieved with removal of occlusive dressing, fasciotomy is indicated. Complete fasciotomy of all compartments with elevated pressures is necessary. AMPUTATION - If there is clinical evidence of compartment syndrome with a probable duration >8 hours, with evidence of muscle necrosis, primary amputation rather than fasciotomy should be considered, following multidisciplinary discussion. CONCURRENT RHABDO Hydration and urinary alkalisation with SODIUM BICARB +/- haemodialysis - Haemodialysis corrects metabolic acidosis and electrolyte abnormalities, and removes plasma myonecrotic toxins. NB: Post-fasciotomy: wound care is important due to the secondary risk of infection and to identify in a timely fashion the presence of necrotic tissue that needs to be debrided; wounds may require covering with skin grafts after the condition of the patient has been optimised. Physical and occupational therapies (with range of motion exercises) are important components of the postoperative treatment.

Answer 149

``` Limb loss Phantom pain Acute renal failure - Myoglobin, which is a breakdown product of muscle cell lysis, is nephrotoxic and can lead to acute renal failure. Sensory deficits Wound infection Motor deficits Psychological effects Volkmann's isachaemic contracture ```

Answer 150

Long-term sequelae of fasciotomy wounds include decreased sensibility, tethered tendons, recurrent ulcerations within the wound closure area, wound infections, and limited motor function of the involved muscles.

Answer 151

compartment syndrome Compartment syndrome may be present at the same time as multiple other injuries, including altered mental status. It is also occasionally associated with intravenous fluid extravasation or aggressive fluid resuscitation.

Answer 152

compartment syndrome Compartment syndrome may be present at the same time as multiple other injuries, including altered mental status. It is also occasionally associated with intravenous fluid extravasation or aggressive fluid resuscitation.

Answer 153

The medial and lateral menisci are shock absorbers and force distributors located between the femur and the tibia. Consequently, menisci can tear due to traumatic injury or degenerative wear (e.g., in knee joint arthritis), and can compromise force distribution across the knee joint. A meniscal tear occurs in 2 primary planes, vertical and horizontal. Tears can cause knee pain, swelling, limited range of motion, and catching, locking, and buckling of the knee joint. Tears may lead to degenerative, arthritic changes if not already present. Can result from playing sport or normal activities of daily living. The athletic population is at greatest risk, especially those who participate in twisting sports (commonly football and basketball). Common complaints include catching, locking, or buckling of the knee, knee pain, or any combination of these symptoms. MRI scan considered most accurate and non-invasive method of diagnosis. Meniscal tears are mainly either traumatic or degenerative. Most tears do not heal spontaneously and are treated arthroscopically by meniscus repair (if torn in a clear, clean pattern) or partial meniscectomy (if torn in a complex or degenerative pattern). Successful outcome requires close follow-up and adherence to physiotherapy.

Answer 154

Traumatic meniscal tears most commonly occur during twisting sports such as football and basketball, but skiers, runners, and tennis players are also at risk. Older patients can tear their meniscus during normal activities of daily living, usually as a consequence of ageing and degenerative wear of the knee joint (knee joint arthritis). The degree of vascular penetration into the periphery of the meniscus ranges from 10% to 25% of the meniscal width. Consequently, most areas of the meniscus cannot heal by themselves because they are not vascularised Additional risk factors include occupations that stress the joint (e.g., construction work and manual labour jobs that involve knee flexion while lifting heavy objects), malalignment of the knee joint, previous ligament injury (especially anterior cruciate ligament injury), and knee instability. Furthermore, it is suggested that increased friction from various sporting turfs may lead to a meniscal tear. Poor ground or weather conditions increase the likelihood of slips, falls, and improper landings, further increasing the risk of meniscal tears

Answer 155

``` STRONG Acute trauma Knee arthritis Knee instability Hx ACL injury Malalignment Rough/uneven playing surface Poor ground Construction work ```

Answer 156

MCMURRAY - Patient is supine with knee in flexion. Examiner flexes the hip and, with one hand on the joint line, rotates the foot internally and externally. Pain with rotation suggests a meniscal tear. This test has low sensitivity and high specificity for diagnosing a meniscal tear APLEY - Patient is prone with knee flexed at 90°. Examiner places axial load on the lower leg while rotating the foot. Patient often feels pain in the affected compartment. POSITIVE HYPEREXTENSION TEST - Examiner lifts the heel of the affected leg, hyperextending the knee and adding additional downwards force on the tibia. Patient reports pain in the affected compartment. Sensitive but not specific for a torn meniscus. Swelling Sensation of instability Knee pain Tenderness at joint line + crepitation

Answer 157

MRI Plane xray if suspect arthritis too

Answer 158

Rest, ice, compression, elevation Physio Analgesia Refractory OR >1cm with root involvement: Surgery - meniscal repair Post op hyaluronic acid possible ________________ Partial meniscectomy: icing and elevation of knee above the level of the heart, use of crutches for first week, and progression to weight bearing as tolerated. Intra-articular hyaluronate injection may decrease post-operative pain and swelling. Meniscal repair: similar to above; however, full weight bearing should be delayed for at least 4-6 weeks and range of movement of the knee, especially full flexion, should be limited to reduce strain on the repair site. Should not return to knee-twisting sports (e.g., football, basketball) for 2 months after meniscal repair.

Answer 159

Spontaneous healing of a peripheral meniscus tear or treatment of the meniscus by repair, reconstruction, replacement, or resection should result in return to full sporting or usual activity. If a tear is not diagnosed early and treated appropriately, a chronic long-standing meniscal tear is the result and is associated with a likelihood of developing degenerative arthritis. After partial meniscectomy Resection leads to rapid recovery over the course of a few weeks. After meniscus repair Surgical repair by suturing requires healing of the torn meniscus, usually taking 4-6 months. After meniscus reconstruction/replacement Meniscal tears treated with these procedures usually take 3 months to heal, with additional maturation occurring over the course of 1 year.

Answer 160

Degenerative arthritis

Answer 161

meniscal tear

Answer 162

meniscal tear

Answer 163

A torn anterior cruciate ligament (ACL) usually occurs as the result of an acute non-contact deceleration injury, forceful hyperextension, or excessive rotational forces about the knee. The ligament may be completely torn, partially torn, or avulsed from its origin or insertion. The ACL is the primary restraint to excessive anterior translation and rotation of the tibia on the femur; therefore, complete ACL disruption typically results in dynamic knee instability or the inability to respond to quick changes in position Injury typified by sudden, painful, audible pop noise. Patient typically presents with inability to return to activity, joint instability, and rapid development of effusion (haemarthrosis). Often tender at lateral femoral condyle, lateral tibial plateau, and tibiofemoral joint lines. A positive Lachman's test is most accurate right after the injury and the pivot shift test is more useful in sub-acute or chronic cases. History and physical examination usually provide accurate diagnosis. X-rays obtained to rule out avulsion fractures or other related conditions, but do not directly identify ACL injury. MRI delineates ACL tears nicely, along with associated injury to menisci and other structures. Initial treatment for most patients consists of protection, rest, ice, compression, elevation, and analgesia (as appropriate). Subsequent treatment varies by an individual patient's health and fitness status and goals. Treatment may range from minimal or no additional intervention to bracing, physiotherapy, and activity modification, and to surgical reconstruction (either early or delayed).

Answer 164

ACL injury occurs when the forces placed upon the ligament exceed its ability to handle those forces. Alternatively, the bony insertion of the ACL may be weaker than the ligament and may avulse from the underlying bone. The ligament may remain intact or may partially tear. Avulsion is most common in children

Answer 165

``` STRONG acute trauma female sex (after puberty) poor technique for landings history of previous ACL injury use of cleats or spikes rough or uneven playing surface ground condition/weather fatigue adolescent, young adults, and middle-aged athletes WEAK aggressive athlete with higher skill level ```

Answer 166

``` Audible pop Rapid swelling Inability to return to activity Pain Instability and buckling +ve lachmans +ve anterior drawer Tenderness at lateral femoral condyle/tiial plateau ```

Answer 167

Ottawa knee rules recommend x-rays in acute knee injury in an adult if any of the following features is present:[56] Inability to bear weight at time of injury and at time of evaluation Isolated tenderness at patella or fibular head Active flexion of knee <90 degrees Age >55. MRI

Answer 168

Sedentary - protected weight bearing/rest/ice/compression/elevation/medicine (PRICEM) + cautious physiotherapy Intense demands - surgical reconstruction: bone-patellar tendon-bone autograft (intra-articular technique) OR hamstring tendon grafts (various bundling/augmentation and tunnelling approaches - intra-articular technique) OR cadaveric allograft (intra-articular technique)

Answer 169

ACL injury used to be considered a career-ending injury for many athletes. However, with surgical reconstruction and proper physiotherapy, 41% to 92% of athletes are able to return to their pre-injury level of activity

Answer 170

``` Bone bruising MCL injury Post traumatic arthritis Meniscal tear Articular cartilage injury ```

Answer 171

ACL tear ACL tears may also occur after slips and falls, twisting injuries to the knee, and high-energy injuries (e.g., motor vehicle accidents). The ACL may be injured alone (isolated) or as part of a more complex injury (multiple ligamentous injuries, meniscal tear, knee dislocation). Complete, intrasubstance tears of the ligament are the most commonly seen injury. Many partial tears involve enough fibres to cause significant instability.[4][5] ACL bony avulsion (tibial eminence) injuries mainly occur in skeletally immature individuals.[6][7] In children, falling off of a bike while trying to plant the ipsilateral foot is a common mechanism of ACL avulsion from the tibial eminence.[8]

Answer 172

ACL tear ACL tears may also occur after slips and falls, twisting injuries to the knee, and high-energy injuries (e.g., motor vehicle accidents). The ACL may be injured alone (isolated) or as part of a more complex injury (multiple ligamentous injuries, meniscal tear, knee dislocation). Complete, intrasubstance tears of the ligament are the most commonly seen injury. Many partial tears involve enough fibres to cause significant instability.[4][5] ACL bony avulsion (tibial eminence) injuries mainly occur in skeletally immature individuals.[6][7] In children, falling off of a bike while trying to plant the ipsilateral foot is a common mechanism of ACL avulsion from the tibial eminence.[8]

Answer 173

The medial collateral ligament (MCL) is a supporting structure on the medial part of the knee joint. Its primary function is to resist valgus (twisting outwards away from the mid-line) and external rotation forces of the tibia in relation to the femur. The mechanism for MCL injury is typically a large valgus and/or external rotation force that is suddenly placed on the knee joint. Injuries to the MCL range in severity from a few torn fibres to complete disunity of the ligament. Occurs when excessive valgus stresses or external rotation forces are placed on the knee joint. The most common symptom is medial-sided knee pain above or below the joint line. Patients are usually able to walk. Diagnosis and grading is primarily made with history-taking and physical examination. Most patients are treated non-operatively. Prognosis for isolated medial collateral ligament injuries is good. Most patients return to sports within 3 to 6 weeks and to pre-injury levels within 3 months. Combined multi-ligament and chronic medial collateral ligament injuries often require operative intervention.

Answer 174

``` Medial knee pain Joint effusion Tenderness Laxity on valgus stress testing Ecchymosis Pop ```

Answer 175

RICE + Physio + NSAIDs Protective ambulation = for grade 1+2 MCL reconstruction or repair with grade 3 or above

Answer 176

Thoracolumbar fractures are breakages in the vertebrae of the spinal column in the thoracic and lumbar regions. They may be associated with disruption of the ligamentous complexes, and can result in instability or compression of neural structures. Thoracolumbar fractures are the usual outcome of thoracolumbar trauma. Other outcomes include traumatic disc prolapse, ligamentous injury, and epidural haematoma causing pressure on the spinal cord or nerve roots; these occur very rarely without a fracture. This monograph focuses on thoracolumbar spine fracture. Usually occurs as a result of high-energy trauma (e.g., road traffic accidents, falls from heights). May occur spontaneously in patients with osteoporotic, neoplastic, or metabolic disorders of the spine. Initial on-the-scene evaluation involves performing primary survey with ABC assessment with C-spine immobilisation and haemorrhage control. It is important to evaluate and assess thoracolumbar fractures for instability. If the decision to operate is made, this should occur earlier rather than later.

Answer 177

The aetiology of traumatic thoracolumbar fractures includes: Motor vehicle accidents (accounts for >50% of fractures)[17] Falls; approximately 3 times more likely to cause fracture in older adults (>65 years of age) than in the younger population (accounts for 25% of fractures)[18] Sports; for example, diving (accounts for 10% of fractures)[17] Gunshot injuries (accounts for 15% of fractures).[19] If fractures occur in younger people with mild trauma, an underlying sinister cause, such as neoplasia (e.g., bony metastasis, multiple myeloma

Answer 178

``` Back pain Bruising Numbness Weakness Spasticity, clonus or hypotonia Hyper or hyporreflexia Hoffmans/babinski Deformity loss of anal sphincter Urinary retention or incontinence Sx of spinal shock - hypotonia that resolves within 24 hrs ``` Absence of s3-4 region - Tested if there is neurological deficit. In males, this involves squeezing the glans penis, and in females it involves applying pressure to the clitoris, and feeling the anal sphincter contract. Absence of this reflex is suggestive of spinal shock, sacral spinal cord injury, or injury to sacral roots.

Answer 179

Thoracolumnar spine x-ray (AP + LATERAL) - fractures; increased inter-pedicular distance, suggesting burst fractures; deformity; subluxation (spondylolisthesis or retrolisthesis) MRI - Useful to identify intra-medullary lesions (e.g., post-traumatic cysts, haematomas, oedema) and extra-medullary compressions (disc, haematoma, bone fragments). Also useful for assessment of posterior ligamentous complex

Answer 180

``` A-E Haemorrhage control Backboardand shine immobilisation Analgesia Replace blood +/- vasopressor ``` May need decompression surgery or surgery, some can be done percutaneously DVT prophylaxis Bladder care Pressure ulcer prevention

Answer 181

``` Complications table COMPLICATION TIMEFRAME LIKELIHOOD  deep spinal infection short term medium  backboard-related pressure ulceration short term low  progressive deformity long term high  chronic pain long term high  deep vein thrombosis variable high  pulmonary embolism variable high  vertebroplasty (VP)- and kyphoplasty (KP)-related complications variable medium  atelectasis and pneumonia variable medium  urinary tract infections variable medium  pedicle screw fixation complications variable medium  muscle injury ```

Answer 182

Lumbar spondylosis refers to degenerative conditions of the lumbar spine that narrow the spinal canal, lateral recesses, and neural foramina. Facet joint and ligamentous hypertrophy, intervertebral disc protrusion, and spondylolisthesis may all contribute to the stenosis, and symptoms result from neural compression of the cauda equina, exiting nerve roots, or both. Patients present with symptoms of neurogenic claudication or radiculopathy. Condition typically resulting from degenerative changes in the lumbar spine. Neurogenic claudication characterised by back and leg pain and lower extremity paraesthesia brought on by ambulation and relieved by sitting. Lumbosacral spine x-rays and computed tomography scans show degenerative changes and possibly spondylolisthesis, but magnetic resonance imaging is the best technique to show neural element compression in the spinal canal and foramina. Initially treated with non-steroidal anti-inflammatory drugs and physiotherapy. Epidural corticosteroid injections may provide symptomatic relief. More severe or persistent symptoms that significantly interfere with function are likely to benefit from decompressive spinal surgery, possibly with fusion if there is degenerative spondylolisthesis or degenerative scoliosis. Neurological deficit including sensory or motor loss occurs in up to 30% of patients, and patients may experience severe morbidity from reduction in the ability to walk.

Answer 183

In nearly all patients, lumbar stenosis is the consequence of degenerative changes in the lumbar spine. With normal ageing, the intervertebral disc loses proteoglycans and water, leading to diminished disc height and circumferential disc bulging. This, in turn, results in altered biomechanical stress on the facet joints leading to facet hypertrophy and thickening of the ligamentum flavum, along with collagen and calcium deposition ``` Age > 40 Back surgery Acromegaly Achondroplasia Manual labour Smoking ```

Answer 184

``` Back pain Onset months-years Activity related Leg pain when walking Stooped posture when walking Numbness/parasthesia Absence of examination findings Sciatica Weakness/wasting ```

Answer 185

Plain xray | MRI

Answer 186

Sig neuro deficit - decompression Non significant Oral corticosteroids/epidural injections Short-term (<4 days) bed rest may be effective in reducing the movements that are perceived as painful by the patient, but it is generally not recommended. Prolonged bed rest may produce stiffness, weakness, and increased pain. Patients should be careful to avoid repetitive bending, lifting, or twisting movements until the pain subsides. Surgery is usually not considered unless symptoms have persisted despite 3 months of medical treatment.

Answer 187

``` Traumatic: Decompressive surgery Corticosteroids VTE prophylaxis Maintenance of volume + BP Prevention of gastric stress ulcers Supportive ``` Non-traumatic intervertebral disc compression aka - Cauda Equina Decompressive laminectomy Malignant Surgery + radiotherapy Abscess Abs +/- surgery

Answer 188

The spectrum of rotator cuff pathology is one of the most common groups of conditions affecting the adult shoulder. Tears can occur with trauma (such as with shoulder dislocation in patients >40 years of age) or be attritional (such as with repetitive overhead activity or chronic degeneration). Shoulder impingement, subacromial bursitis, rotator cuff syndrome, and rotator cuff tendonitis all overlap and can be a continuum of terminology representing similar pathology. Common shoulder condition, especially in older and active people. Tears can be symptomatic or asymptomatic. Cause of tear can be traumatic or attritional. Treatment typically based on degree of dysfunction, pain, and quality of tendons and muscles of the rotator cuff, as well as patient goals and activity level. In patients with lower functional demands, rehabilitation therapy, including ROM and strengthening exercises, is critical to return patients to better function. A subacromial injection can alleviate pain. If higher activity level is desired or the tear is acute, surgical intervention has a better functional result than non-operative treatment.

Answer 189

Multiple studies have illustrated the direct correlation between incidence of tears and increasing age. In one study, MRIs performed in 96 asymptomatic patients found a 34% overall prevalence of rotator cuff tears (28% in patients ≤60 years old and 54% in patients >60 years old).[1] Another study found similar results using ultrasound in 411 asymptomatic volunteers: 23.4% overall prevalence and 38% prevalence for patients older than 60 years.[2] No other significant differences or trends in epidemiology are known.

Answer 190

Rotator cuff tears can result from an acute traumatic event, repetitive or vigorous overhead activity (such as throwing a baseball or painting), or chronic degeneration. They can be considered the final stage of a continuum of pathology and clinical symptoms referred to as subacromial impingement syndrome. The space between the undersurface of the acromion and the superior aspect of the humeral head (the impingement interval) is maximally narrowed in a normal patient with abduction of the shoulder. Impingement can result from any condition that further narrows this space. Anatomically, this space is affected by the morphology of the undersurface of the acromion: type I (flat), type II (curved), and type III (curved with an anterior hook). Extrinsic compression or loss of rotator cuff competency can lead to impingement. For example, cadaveric studies have described an increased incidence of rotator cuff tears in patients with a type II or III acromion. Tears associated with chronic impingement syndrome start on the bursal surface or within the tendon substance. A common factor leading to impingement is diminished tendon blood supply due to ageing. Because of the poor blood supply in the area along the rotator cuff insertion and the critical stresses placed on this area, attritional and intrinsic tears commonly begin in this location along the supra- and infraspinatus.

Answer 191

STRONG Age >60 WEAK Hx repetitive overhead movement Hx of superior labral tears Shoulder injury

Answer 192

Shoulder pain Weakness loss of ACTIVE ROM Pain on external rotation test - INFRASPINATUS Empty can - SUPRSPINATUS Belly press - SUBSCAPULARIS Scarf test - ACROMIOCLAVICULAR JOINT Hawkins impingement test - The patient's arm is positioned in 90° of elevation and the elbow is bent to 90°. The examiner places an internal rotation force on the patient's arm. Reproduction of pain is a positive test for impingement. IMPINGEMENT Neer impingement test - The Neer impingement test can be performed with the patient seated or standing. The examiner keeps one hand on the patient's scapula to prevent rotation. As the patient's arm is elevated by the examiner, reproduction of pain is a positive test for impingement. Deltoid pain Adhesive capsulitis ('frozen shoulder') is defined as the symmetrical loss of both passive and active motion due to soft-tissue contracture. Loss of passive shoulder motion is uncommon in the presence of large or massive rotator cuff tear. Stiffness can occur with massive chronic tears as a result of injury or failure to move the shoulder (prolonged immobilisation).

Answer 193

X-ray - usually normal; may show opacities if calcific tendonitis present; may show superior migration of the humeral head relative to the glenoid (large or massive tears); may show pseudosubluxation of the humeral head inferior to the glenoid (acute massive tears) Possible to perform diagnostic injection-To distinguish true weakness from weakness caused by pain, a pain-relieving injection of 1% lidocaine into the subacromial bursa should be followed by retesting of rotator cuff strength. MRI

Answer 194

ACUTE TEAR (ie within 6w) Tear + young patient - surgery Options include arthroscopic, mini-open, and open repair. Physio post op

Answer 195

``` Rotator cuff arthropathy NSAID Gi events Re-rupture Post op septic arthritis Adhesive capsulitis ```

Answer 196

rotator cuff injury

Answer 197

Shoulder impingement syndrome occurs when the tendons of the rotator cuff and the subacromial bursa are pinched in the narrow space beneath the acromion. This causes the tendons and bursa to become inflamed and swollen. This pinching is worse when the arm is raised away from the side of the body. Impingement may develop over time as a result of a minor injury, or as a result of repetitive motions that lead to inflammation in the bursa. Particular shapes of the acromion may make certain individuals more susceptible to impingement problems between the acromion and the bursa. With age and the onset of arthritis, the acromion may develop bone spurs that further narrow this space. Impingement caused by bone spurs on the acromion is common in older patients who participate in sports or work activities that require overhead positions. Spurs may also result if one of the ligaments in the coracoacromial arch becomes calcified. Impingement is classified in three grades: Grade I is marked by inflammation of the bursa and tendons Grade II has progressive thickening and scarring of the bursa Grade III occurs when rotator cuff degeneration and tears are evident

Answer 198

Shoulder impingement syndrome occurs when the tendons of the rotator cuff and the subacromial bursa are pinched in the narrow space beneath the acromion. This causes the tendons and bursa to become inflamed and swollen. This pinching is worse when the arm is raised away from the side of the body. Impingement may develop over time as a result of a minor injury, or as a result of repetitive motions that lead to inflammation in the bursa. Particular shapes of the acromion may make certain individuals more susceptible to impingement problems between the acromion and the bursa. With age and the onset of arthritis, the acromion may develop bone spurs that further narrow this space. Impingement caused by bone spurs on the acromion is common in older patients who participate in sports or work activities that require overhead positions. Spurs may also result if one of the ligaments in the coracoacromial arch becomes calcified. Impingement is classified in three grades: Grade I is marked by inflammation of the bursa and tendons Grade II has progressive thickening and scarring of the bursa Grade III occurs when rotator cuff degeneration and tears are evident

Answer 199

Complex regional pain syndrome (CRPS) is defined as continuing (spontaneous and/or evoked) regional pain that is out of proportion to the severity of the inciting event and beyond the normal time frame expected following the event. The pain is usually regional (not in a specific nerve territory or dermatome) and has a distal predominance of abnormal sensory, motor, sudomotor, vasomotor, and/or trophic findings with variable progression over time. Prolonged pain, disproportionate to the initiating event, most frequently following minor trauma and most commonly affecting the distal aspect of an extremity. Pain often described as spontaneous, burning, lancinating, sharp, shooting, or electric. Characteristically develops dull, boring, and aching qualities with chronicity. Allodynia and hyperalgesia are almost always present. Local oedema, erythema, sweating abnormalities, and trophic skin and nail changes are often, but not always, present. The affected extremity is often held immobile, and this can be associated with dystonia, focal weakness, and contractures. Diagnosis is clinical. No specific tests are diagnostic; investigations may be useful to support the diagnosis or rule out alternative pathology. The treatment goal is functional restoration of a limb by using adequate pain management techniques, with patient education, physiotherapies, pharmacotherapy, and appropriate psychological techniques tailored to the individual patient.

Answer 200

There are no specific tests to confirm CRPS. It is principally a clinical diagnosis. Investigations may support the diagnosis or rule out differentials.

Answer 201

``` Physio Pred Bisphosphonates TCA Anticonvulsants Local anaesthetic Sympathetic nerve block ```

Answer 202

Reduction, immobilisation and rehabilitation

Acute Flashcards

(228 cards)