Acute and emergency (Anki)

Describe the pathophysiology of saliclyate overdose (aspirin)

Mild toxicity - salicylates directly irritate the gastric lining Higher doses - Mixed respiratory alkalosis and metabolic acidosis Severe toxicity - salicylates stimulate the cerebral medulla, leading to hyperventilation and respiratory alkalosis.

In salicyate poisoning, the metabolisation of salicylates causes what?

Results in anaerobic metabolism- This causes heat production, pyrexia and metabolic acidosis (due to lactate production) This leads to hyperventilation (compensation)

What are the mild symptoms of saliycate overdose? (mild)

Nausea Epigastric pain Tinnitus Dizziness Lethargy

What are the symptoms of severe salicylate toxicity?

Confusion Convulsions Coma

Upon clinical examination, what are the findings of salicyate poisoning?

Warm peripheries and bounding pulse Tachypnoea and hyperventilation Cardiac arrhythmia Acute PE

What are the relevant bedside investigations for suspected salicylate poisoning?

1) Obs (common tachypnoea + Tachycardia) 2) ECG - monitor for arrhythmias (esp QRS / QT prolongation) 3) Arterial blood gas - monitor acid-base balance.

What are the relevant laboratory investigations for suspected salicylate poisoning?

1) Plasma saliclyate conc- taken at least 2 hours after ingestion and repeated every 2 hours until salicylate conc peaks. 2) Plasma paracetamol conc - just incase mixed overdose 3) FBC - exclude infetion 4) U&Es - Hyperkalaemia is common. Urea and Creatinine could be raised - AKI 5) LFTs - assess hepatic dysfunction 6) Coagulation - INR and prothrombin time may be increased if hep dysfunction.

Describe the managment of salicylate overdose:

1) Activated charcoal - within 1 hour 2) IV fluid resus 3) Potassium replacement 4) Sodium bicarb - reduces CNS transfer and enhances urinary excretion.

Ongoing management for salicyate overdose?

What are the complications of salicyate overdose?

ARDS SEIZURES - use bendodiazepines (e.g. lorazepam) Drug induced hepatitis Cardiac arrest - prolongation of QT common

Classification of burns: 1) What is a superficial burn? 2) Management?

1) A superficial burn will typically result in blistering. Deroofing of these blisters will reveal pink and blanching skin underneath. 2) Silver based dressings - urgotul, Paraffin for facial burns

Classification of burns: What is a Partial-thickness burn? Management?

- Damage to the superficial capillaries supplying the skin. - The deeper areas will have fixed staining on palpation, and the deepest areas will be paler, and may not blanch at all. - Will be managed conservatively with dressings e.g Flamazine

Classification of burns: What is a full-thickness burn?

Full-thickness burns will commonly present as white and insensate. If the burn has extended beyond the subcutaneous fat, the skin may appear charred and shrunken. Requires excision, with coverage with a split-thickness skin grafts. Will not heal with dressings.

What is the management of a severe burn?

Managed using ABCDE approach Inhalation burns can cause larygneal oedema, so early intubation.

The percentage surface area of a burn is calcualated by? The fluid requiremenets are caclulated by? When should fluid resus commence for adults and children?

Wallace's rule of 9s Parkland formula Adults - if burn exceeds 15% Children - if burn exceeds 10%

Describe the ongoing managment of a serious burn

- Debride the burn thoroughly - - All dead tissue removed to avoid sepsis. - Keep patient warm (loss of SA, more fluid lost through evaporation) - Specialist burns unit

Describe the rehab process of a serious burn

Extubation High calorie diet to rebuild tissue Physiotherapy and scar massage Psycological help

What are the symptoms of sepsis?

Localising symptoms of infection e.g productive cough, vomiting, diarrhoea, dysuria) Drowsiness Confusion Dizziness Malaise

What are the red flags for sepsis? (ABCDE)

B - resp rate >25 Oxygen required to keep SPO2 >92% C- HR >130bpm SBP

Describe the management of Sepsis

SEPSIS 6: Administer high flow oxygen to maintain spo2 >94 Blood cultures Measure serial lactate levels Adminster IV fluids Monitor urine output (all boys m and m)

What investiagtions would be neededd for sepsis? Blood tests:

Blood tests: FBC - Rule out anaemia and raised wbc typical in sepsis U&Es - Assess renal function CRP - raised in sepsis Lactates - Assess for evidence of reduced end-organ perfusion Coagulation - assess for DIC Blood cultures - Isolate causative organism

Investigations for sepsis: VBG?

Serum glucose level Lactate

What are the interventions for sepsis?

Broad spectrum IV antibiotics Intravenous fluids

What is this?

Livedo Reticularis - 'mottling' Clinical context - can be sign of severe sepsis or DIC (can be non pathological in babies and children)

What about his history suggest signs of evere sepsis?

Tachycardic Hypotensive Febrile (fever) Evidence of end organ dysfunction ( low urine output and confusion)

What kind of rhythm is this? Treatment?

Aystole - flat line but has a wandering baseline CPR and adrenaline evry 3-5 mins

What is type 1 respiratory failure?

pO2

What obs would be seeen in type 2 respiratory failure?

pO2 < 8 and high pCO2

What is the management of hypertension for

Ace inhibitor / angiotensin 2 receptor blocker step 2 = A + Calcium channel blocker or A + Diuretic (thiazide) step 3 = A + C + D

VTE prophlyaxis: What are the contraindications?

Active bleeding Exisiting anticoagulation with warfarin or a NOAC.

Describe the presentation of a PE

- SOB - Normal cough or haemopytisis - Hypoxia - Tachycardia - Tachypnoea - Low grade fever - Haemodynamic instability causing hypotension Also may be signs of a DVT (uniliateral leg swelling/ tenderness)

Describe the diagnosis of PE

If wells score likely: CT pulmonary angiogram or VQ scan

What are the typical findings on an ABG with a PE?

Respiratory alkalosis This is becuase the high resp rate reduces co2. Patients with a PE will also have a low pO2..

Describe the managment of PE

Oxygen as required Analgesia if required Intial managment plan: 1) Apixaban or rivaroxaban 2) LMWH as an alternative when not suitable, or in antiphospholipid syndrome. (e.g. enoxaparin and dalteparin) Should be started immediately before conforming diagnosis when DVT/PE suspected and there is a delay in getting the scan.

Long term anticoagulation in VTE?

Warfarin / NOAC / LMWH 1) Warfarin 2) NOACs/DOACs as an alterantive for anticoagulation that doesnt require monitoring 3) LMWH first line treatment in pregnancy or cancer.

Describe the treatment that is used when there is a massive PE with haemodynamic compromise. Examples?

Thrombolysis - injecting a fibrinolytic medication that rapidly dissolves clots. Streptokinase, alteplase and tenecteplase

When a patiennt presents with possible ACS symptoms, what ECG findings would suggest a STEMI?

ST elevation or New left bundle branch block.

Describe the diagnosis of an NSTEMI

ACS symptoms 1) If no ST elevation on ECG, then perform troponin blood tests 2) If troponin raised AND other ECG changes - ST depression / T wave inversion or pathological Q waves, the diagnosis is NSTEMI.

ECG changes in NSTEMI?

ST segment depression in a region Deep T wave inversion Pathological Q waves (suggests a deep infarct - late sign)

A rise in troponin is consistent with what?

Myocardial ischaemia - as the proteins are released from ischaemic muscle They are non-specific, meaning that a raised troponin does not automatically mean ACS.

What investigations (bloods) for MI?

Physical Examination (heart sounds, signs of heart failure, BMI)ECGFBC (check for anaemia)U&Es (prior to ACEi and other meds)LFTs (prior to statins)Lipid profileThyroid function tests (check for hypo / hyper thyroid)HbA1C and fasting glucose (for diabetes) Plus:Chest xray to investigate for other causes of chest pain and pulmonary oedemaEchocardiogram after the event to assess the functional damageCT coronary angiogram to assess for coronary artery disease

Describe the treatment for an acute STEMI

Primary PCI (within two hours of presentation) Thrombolysis (if PCI not available within 2 hours)

Describe the treatment for an acute NSTEMI

Beta blockers Asprin 300mg stat dose Ticagrelor 180mg stat dose (clopidogrel if higher bleeding risk) Morphine tritrated to control pain Anticoaguant : Fondaparinux (unless high bleeding risk) Nitrates e.g. GTN to relieve coronary artery spasm

What are the complications of MI

D – Death R – Rupture of the heart septum or papillary muscles E – “Edema” (Heart Failure) A – Arrhythmia and Aneurysm D – Dressler’s Syndrome

What is Dressler's Syndrome? Diagnosis? Management?

- Also called post-myocardial infarction syndrome - Usually occurs 2-3 weeks after an MI - Caused by a localised immune response and causes pericarditis. Diagnosis ECG: ST elevation and T wave inversion Echocardiogram: Pericardial effusion FBC: Raised inflammatory markers CRP and ESR Management: - NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). (may need pericardiocentesis to remove fluid from around the heart)

What is a pneumothorax? Causes? Typical patient in exams?

Occurs when air gets inside the pleural space, separating the lung from the chest wall. It can occur spontaneously, or secondary to trauma, medical interventions or lung pathology. Tall thin young man, presenting with sudden breathlessness and pleuritic chest pain, possibly while playing sports

What investigations are needed for a supsected pneumothorax?

Erect chest x ray

Describe the presentation of a pneumothorax on an erect chest x ray

Area between the lung tissue and the chest wall, where there are no lung markings. There will be a line demarcating the edge of the lung where the lung markings end and the pneumothorax begins .

Describe the managment of a Pneumothorax

1) No shortness of breath and less than 2cm rim of air on the chest x-ray: - No treatment is required as it will spontaneously resolve, follow up in 2-4 weeks 2) Shortness of breath and more than 2cm rim of air on x ray: - Aspiration followed by reassessment - When aspiration fails twice, a chest drain is required. 3) Unstable patients, bilateral or secondary pneumothoraces generally require a chest drain.

What are the signs of a Tension pneumothorax?

Tracheal deviation away from the side of the pneumothorax Reduced air entry on the affected side Increased resonance to percussion on the affected side Tachycardia Hypotension

Describe the management of a tension pneumothorax

1) Insert a large bore cannula into the second intercostal space in the midclavicular line 2) Once the pressure is relieved with the cannula, then a chest drain is required for definitive managment.

Describe the pathophysiology of a Tension pneumothorax

- Caused by trauma to the chest - Creates a one-way valve that lets air in but not out of the pleural space. - Creates pressure inside the thorax that will push the mediastinum across, kink the big vessels in the mediastinum and will cause cardiorespiratory arrest.

Pneumothorax: Describe how a chest drain is performed

Inserted in the triangle of safety: - 5th intercostal space (inferior nipple line) - Midaxillary lline (lateral edge of latissiumus dorsi) - Anterior axillary line (Lateral edge of pectoralis major)

What is Hyperglycaemic hyperosmolar non-ketotic syndrome?

Life threatening complication of uncontrolled diabetes mellitus. Syndrome characterised by severe hyperglycaemia Marked increase in serum osmolality and dehydration no ketoacidosis

Describe the managment of Hyperosmolar non-ketotic state

IV 0.9% sodium chloride to restore circulating volume and reverse dehydration IV insulin (low dose) Correct other electrolyte deficiencies

What is the underlying pathology of SJS and TEN? Difference between SJS and TEN?

Disproportional immune response causes epidermal necrosis, resulting in blistering and shedding of the top layer of skin. SJS -

What are the medications that can cause SJS and TEN?

Anti-epileptics Antibiotics Allopurinol NSAIDs

What are the infections that are able to cause SJS and TEN?

Herpes simplex Mycoplasma pneumonia Cytomegalovirus HIV hear my cat hiss

Describe the presentation of SJS and TEN

Patients usually start with non specific symptoms of fever, cough, sore throat and sore mouth Then develop a purple/red rash that spreads across the skin and stars to blister Skin starts to break away and shed, leaving the raw tissue underneath.

Describe the managment of SJS and TEN

Patients should be admitted to suitable dermatology/burns unit for treatment Good supportive care - nutrition, antiseptics, analgesia and opthamology input Treatment - steroids, immunoglobulins, immunosuppressant

Describe the complications of TEN and SJS

Secondary infection: The breaks in the skin can lead to secondary bacterial infection, cellulitis and sepsis. Permanent skin damage: Skin involvement can lead to scarring and damage to skin, hair, nails, lungs and genitals. Visual complications: Depending on the severity, eye involvement can range from sore eyes to severe scarring and blindness.

What is meningitis?

Inflammation of the meninges - lining of the brain and spinal cord. Due to bacterial/viral infection.

What is rhe cause of the 'non-blanching rash' in a Meningitis infection?

Caused by meningococcal septicaemia - when the meningococcus bacterial infection is in the bloodstream. The infection at this point has caused DIC and subcutaneous haemorrhages.

What is the most common cause of bacterial meningitis in children and adults? Neonates?

Neisseria meingitis (meningococcus) and Streptococcus pneumonia (pneumococcus) Group B streptoccocus

Describe the presentation of meningitis

Fever Vomiting Headache Photophobia Altered consciousness Seizure Non blanching rash in meningococcal septicaemia

Tests to look for meningeal irritation: What is Kernig's test?

Patient lying down, flex one hip and knee to 90 degrees, and then slowly straightening the knee whilst keeping the hip flexed. There will be pain/resistance if positive.

Tests to look for meningeal irritation: What is Brudzinski's test?

Patient lying flat on their back and lift their head and neck of the bed and flex chin to chest. Positive test - causes patient to involuntarily flex their hips and knees.

What are the non-specific signs indicating meningitis in neonates and babies? What must be done as a part of the investigation for all children?

Bulging fontalle, hypotonia poor feeding lethargy hypothermia Lumbar puncture

Describe the management of Bacterial Meningitis - Community?

Benzylpenicillin prior to transfer to hospital

Describe the management of Bacterial Meningitis - Hospital? Antibiotics used? If risk of penicillin resistant pneumococcal infection?

1)Blood culture and lumbar puncture prior to starting antibiotics, however if patient is acutely unwell antibiotics should not be delayed. 2) Blood tests for meningococcal PCR if meningococcal disease is suspected Antibiotics: < 3 months - cefotaxime + amoxicillin > 3 months - ceftriaxone Vancomycin should be added + Steroids in bacterial meningitis (dexamethasone)

Post exposure prophylaxis for meningits?

The usual antibiotic choice for this is a single dose of ciprofloxacin. It should be given as soon as possible and ideally within 24 hours of the initial diagnosis.

What are the most common causes of viral meningits? Managment?

HSV, Enterovirus, VSV A sample of the CSF from the LP should be sent for viral PCR testing. Viral meningitis usually milder, only supportive treatment, but for HSV meningitis - Aciclovir.

CSF for bacterial meningits?

CSF for viral meningits?

Describe the managment of STEMI

What is inflammatory bowel disease?

Term for Ulcerative colitis and Crohns disease

What are the distinct features of Crohns disease? Associated feautures?

"N- No blood or mucus E- Entire GI tract S - ""Skip lesions' on endoscopy T- Terminal ileum most affected and transmural (full thickness) inflammation S- Smoking is a risk factor Associated with weight loss, strictures and fistulas."

What are the distinct features of Ulcerative Colits?

Ulcerative Colitis (remember U – C – CLOSEUP) C - Continuous inflammation L - Limited ONLY to colon and rectum O - Only superficial mucosa affected S - Smoking is protective E - Excrete blood and mucous U - Use aminosalicylates P - Primary sclerosing cholangitis

Describe the presentation of Ulcerative colitis

- Diarrhoea - Abdominal pain - Passing blood - Weight loss

Describe the testing needed for Ulcerative colitis

- Routine bloods for anaemia, infection, thyroid, kindey and lvier function - CRP indicates inflammation and active disease - Faecal calprotectin (released by inflamed intestines) useful screeing test for IBD - Endoscopy - Imaging with ultrasound, CR and MRI can be used to look for complications (fistulas, abcesses and strictures)

Describe the management of Crohns

Inducing remission : Steroids (oral prednisolon / iv hydrocortisone) if these dont work then immunosuppressants Maintaing remission: Axathioprine Mercaptopurine

What is rhabdomyolisis? Causes?

Skeletal muscle tissue breaks down and releases breakdown products into the blood. Extreme underuse or a traumatic injury

1) What is the immediately dangerous breakdown product of rhabdoymyolisis 2) what can this cause? 3) What can cause AKI?

Potassium Hyperkalaemia can cause cardiac arrhythmias that can lead to cardiac arrest. Myoglobin - the AKI causes the breakdown products to further accumulate in the blood

What are the signs and symptoms of rhabdomyolisis?

Muscle aches and pain Oedema Fatigue Confusion Red brown urine

What are the investigations needed for suspected rhabdomyolisis?

Creatine Kinase (CK) - Will be very high, and remains elevated for 1-3 days. Urine dipstick - Will test positive for blood due to myoglobinurea ECG - To assess hearts response to hyperkalaemia.

Describe the managment of rhabdomyolisis

IV fluids - rehydration and encourages filtration of breakdwon products IV sodium bicarbonate - Aims to make the urine more alkaline and reduces the toxicity of the myoglobin on the kidneys IV mannitol - Increases glomerular filtration rate to flush breakdown products and reduce oedema surrounding muscles and nerves. Treat hyperkalaemia

What are the symptoms of toxic megacolon?

Swelling of the belly Pain in the belly Fever Rapid heart rate Shock Diarrhea

Describe the treatment of toxic megacolon

Anti-inflammatory medicines can help control inflammation, antibiotics can hep or treat infection Bowel rest/decompression - removes gas IV fluids Surgery - remove part/ or all of the colon.

What is compartment syndrome?

Where pressure within a fascial compartment is abnormally elevated, cutting off blood flow to the contents of the compartment.

What urgent surgery is needed for acute compartment syndrome? What could happen without prompt treatment?

Fasciotomy - relieves pressure within the compartment and restores blood flow Tissue necrosis and permanent damage

What two injuries does acute compartment syndrome usually present after?

Bone fractures Crush injuries

Describe the presentation of compartment syndrome (five symptoms)

5 Ps Pain Parasthesia Pale Pressure Paralysis (late and worrying feature)

Typical presentation of comparment syndrome in exams?

Disproportionate pain, medications are not effective with patients after an injury

What is the management of acute compartment syndrome?

Needle manometry to measure compartment pressure (manometer measures resisitance to injecting saline through a needle into the compartment) Emergency fasciotomy

What is a bowel obstruction? A bowel obstruction results in what?

Refers to when the passage of food, fluids and gas through the intestines becomes blocked. Obstruction results in a build up of gas and faecal matter proximal to the obstruction (befire)

Why does bowel obstruction cause vomiting?

Build up of gas and faecal matter causes back-pressure resulting in dilatation of the intestines proximal to the obstruction.

What are the three main causes for bowel obstruction?

1) Adhesions (small bowel) 2) Hernias (small bowel) 3) Malignancy (large bowel)

What are bowel adhesions? Typically causes large or small bowel obstruction?

Adhesions are pieces of scar tissue that bind abdominal contents together, cause kinking or squeezing of the bowel, leading to mainly small obstruction.

What are the causes of intestinal adhesions?

Abdominal or pelvic surgery Peritonitis Abdominal or pelvic infections (e.g. PID) Endometriosis

What is a closed loop bowel obstruction? Causes? What are the dangers of closed-loop obstruction

Where there are two points of obstruction along the bowel. Adhesions (compress two areas of bowel) Hernias (isolate a section of bowel blocking either end) Volvulus (where the twist isolates a section of intestine) Closed loop section of bowel do not have an open end where they can drain and decompress. Therefore section will continue to expand leadinf to ischaemia and perforation. Requires emergency surgery.