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Turner syndrome

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Turner syndrome affects females and is due to the partial or total absence of one X chromosome. 

Incidence is around 1 in 3000 live female births

Features include:
  • Congenital heart defects – occur in 1/3; most commonly
  • Short stature 
  • Widely-spaced nipples 
  • Webbed neck 
  • Prominent ears 
  • Short fourth metacarpals 
  • Cubitus vulgaris 
  • Lack of spontaneous puberty
  • Congenital lymphoedema 

Complications associated with Turner syndrome include 
  • Osteoporosis
  • Sensorineural hearing loss
  • Aortic root dilation

Diagnosis is by karyotyping 


References 

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Porphyria

/ / / / /
Porphyrias are inherited disorders of haem synthesis resulting in the accumulation of porphyrin and porphyrin precursors. 

There are 7 main types of porphyria; only 3 are considered here. 

  • Acute intermittent porphyria
    • Caused by a defect of porphobilinogen deaminase 
    • Most common in those around the age of 30
    • Females > males 5:1
    • Autosomal dominant inheritance, although only 10 to 20% of carriers become symptomatic 
    • Signs/symptoms may include
      • Abdominal pain
      • Tachycardia
      • Muscle weakness
      • Sensory changes in a ‘bathing suit’ distribution
      • Constipation
      • Nausea and vomiting
      • Postural hypotension
      • Hypertension
      • Low sodium 
      • Seizures 
      • Paralysis
      • Psychosis
    • Precipitants 
      • Medications – sulphonamides, methyldopa, danazol, diazepam, phenytoin, carbamazepine, sulphonylureas, chloramphenicol, tetracyclines, some anthistamines
      • Alcohol 
      • Illicit drugs – cocaine, amphetamines, ecstasy, marijuana
      • Fasting
      • Stress
      • Infections 
      • Smoking 
      • Pregnancy
      • Pre-menstrual hormone variation
    • Diagnosis
      • Urine dark on standing due to polymerisation of porphobilinogen to porphyrins 
      • Urinalysis of urine protected from light looking for raised aminolaevulinic acid and porphobilinogen
    • Management of acute attacks
      • Pain relief – opiates if required
      • Convulsions managed with gabapentin or vigabatrin
      • Monitor sodium – if low, fluid restrict 
      • Glucose 
      • Haem arginate - slow IV infusion 

  • Variegate porphyria 
    • Causesd by a mutation in the gene for protoporphyrinogen oxidase 
    • Most common in South Africans 
    • Features 
      • Cutaneous manifestations 
        • Photosensitive blistering
        • Hyperpigmentation
      • Abdominal pain
      • Dark urine 
      • Neuropsychiatric symptoms 

  • Porphyria Cutanea Tarda 
    • This is the commonest of all the porphyrias 
    • 2 forms – sporadic (around 90%) and familial (10%)
    • It is caused by a mutation in the gene encoding uroporphyrinogen decarboxylase 
    • Features
      • Light-sensitive dermatitis – blisters 
      • Hypertrichosis
      • Often iron overload 
      • Urine glows pink under Wood’s lamp due to raised uroporphyrinogen
    • Precipitants of attacks include 
      • Alcohol 
      • Iron 
      • Oestrogens 
      • Sunlight
    • Associations
    • Treatment: 
      • Avoidance of sunlight
      • Oral chloroquine
      • Venesection

References

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Lesch-Nyhan Syndrome

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Lesch-Nyhan Syndrome is a recessive x-linked disorder caused by a mutation in the HPRT gene encoding hypoxanthine guanine phosphoribosyltransferase, which results in increased levels of uric acid.

Features include:
  • Mental retardation 
  • Self-mutilation – biting fingers and lips 
  • Orange crystals in nappies 
  • Gout 
  • Megaloblastic anaemia

Management: allopurinol 

Prognosis: death in 20s/30s


References 

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COPD

/ / / /
Chronic Obstructive Pulmonary Disease (COPD) is characterised by airflow obstruction that is not fully reversible, with a reduced FEV1/FVC ratio of less than 0.7. 


NICE recommends that a diagnosis of COPD is considered in patients older than 35 with a risk factor (generally smoking) who present with one or more of the following: 
  • exertional breathlessness
  • chronic cough
  • regular sputum production
  • frequent winter ‘bronchitis’ 
  • wheeze 


Investigations 
  • Spirometry - obstructive pattern; done post bronchodilator
    • Severity of COPD
      • Mild – FEV1 ≥ 80% predicted
      • Moderate – FEV1 50 – 79% predicted
      • Severe – FEV1 30 – 49% predicted 
      • Very severe – FEV1 <30% predicted or < 50% predicted with respiratory failure 
  • CXR
  • FBC - looking for polycythaemia/anaemia
  • BMI calculation 


Management

  • General management 
    • Stop smoking 
      •  Offer NRT, varenicline or bupropion
    • Medications
      • Inhaled therapy
        • Short-acting beta 2 agonists (SABA) for symptomatic relief
        • Preventative therapy:
          • FEV1 ≥ 50% predicted: long-acting beta 2 agonist (LABA) or long-acting muscarinic antagonist (LAMA) 
          • FEV1< 50% predicted: either LABA with inhaled corticosteroid or LAMA 
      • Oral theophylline if patient unable to use inhalers or in addition to if adequate control not achieved with inhalers
        • Plasma levels must be monitored 
        •  Dose must be reduced if macrolide or fluroquinolone antibiotics prescribed
      • Mucolytic drugs
  • Long term oxygen therapy
    • Indications:
      • PaO2 less than 7.3kPa in stable COPD
      • PaO2 less than 8kPa if stable and one of:
        • secondary polycythaemia
        • nocturnal hypoxaemia (=sats <90% for more than 30% of the time)
        • peripheral oedeam
        • pulmonary hypertension
      • Need at least 2 ABGs done at least 3 weeks apart
      • Need O2 for 15 hours per day, greatest benefits if used for 20 hours per day
  • Consider lung volume reduction surgery 
    • If single large bulla on CT and FEV1 <50% predicted or
    • breathless and marked restriction in daily living and all of the following criteria met:
      • FEV1 more than 20% predicted
      • PaCO2 less than 7.2 kPa
      • upper lobe predominant emphysema
      • TLCO more than 20% predicted

  • Management of an exacerbation
    • Oral corticosteroids – prednisolone 30mg od for 7 to 14 days 
    • Nebulised salbutamol and ipratropium bromide
    • If infective, antibiotics – empirically a macrolide or tetracycline
    • IV theophylline if inadequate response to nebulisers
    • NIV for persistent hypercapnic ventilatory failure
      • Consider if ongoing acidosis after one hour of standard medical treatment
      • If pH <7.26 higher risk of NIV failure so should be managed in high dependency setting 
      • Initial IPAP 10cm H20, titrated in increments of around 5cm H20 each 10 minutes to usual target IPAP of 20cm H20
      • EPAP 4-5cms H2O 
      • ABGs at 1 hour, 4 hours and 12 hours as a minimum 
Last updated: April 2013

Small print gem: spacers should not be cleaned more than monthly and should be allowed to air dry. Frequent cleaning or towel-drying decreases their effectiveness due to a build-up of static 


References:

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Warfarin

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Warfarin is an anticoagulant that works by inhibiting vitamin K epoxide reductase, which prevents vitamin K being recycled. As vitamin K is essential for the activation of factors II, VII, IX and X this decreases coagulation.

However, vitamin K is also a cofactor for protein C and protein S, both of which are inhibitors within the clotting cascade. They also have shorter half-lives than factors II, VII, IX and X. Therefore, warfarin is initially a procoagulant.

Indications for warfarin therapy include: 
  • Venous thromboembolism (DVT/PE) 
    • Target INR 2.5 (unless recurrent VTE whilst on anticoagulant, in which case target INR = 3.5) 
    • Start with heparin cover which should be continued for at least 5 days and until INR ≥ 2 for at least 24 hours, whichever is longer 
    • Duration of treatment with warfarin 
      • Proximal DVT (= popliteal vein or above) or PE: 3 months
      • Isolated calf vein DVT: 6 weeks 
    • Cancer-associated VTE: 6 months with therapeutic LMWH rather than warfarin
  • Atrial fibrillation 
    • Warfarin is not required for all AF patients 
    • If it is, target INR = 2.5 
  • Prosthetic heart valves 
    • Mechanical valves 
      • Target INR depends on valve and risk factors 
      • Risk factors: 
        • valve in mitral, tricuspid or pulmonary position
        • AF 
        • Left atrium diameter >50mm 
        • Mitral stenosis
        • LVEF <35%
      • Examples of valve types and INR
        • St Jude Medical – INR 2.5 if no risk factors, INR 3.0 if risk factors 
        • Starr-Edwards – INR 3.5 
    • Bioprosthetic valves 
      • Some require initial anticoagulation with warfarin 
  • Elective cardioversion 
    • Anticoagulate for 3 weeks prior to procedure and 4 weeks post
    • Target INR 2.5 
  • Mitral stenosis or regurgitation 
    • If warfarin indicated, target INR 2.5 

Warfarin is metabolised by cytochrome P450. 

Interactions with warfarin which may result in a raised INR include: 
  • Medications 
    • Antibiotics 
      • Metronidazole 
      • Erythromycin
      • Clarithromycin
      • Ciprofloxacin
      • Tetracyclines 
    • Allopurinol 
    • Amiodarone 
    • SSRIs 
    • Fluconazole
    • Cimetidine 
    • Omeprazole
  • Drinks 
    • Cranberry juice 
    • Alcohol 
  • Hyperthyroidism 

Interactions with warfarin which may result in a lower INR include
  • Rifampacin 
  • St Johns Wort 
  • Carbamazepine 
  • phenyotin 

Management of high INR
  • Major bleeding 
    • Prothrombin complex concentrate 
    • 5mg IV vitamin K 
    • FFP is suboptimal and should only be used if prothrombin complex is not available 
  • Non-major bleeding 
    • 1-3mg IV vitamin K
  • Non-bleeding INR > 8.0
    • 1-5mg oral vitamin K
  • Non-bleeding INR >5.0 
    • Withhold 1-2 doses of warfarin 
    • Reduce subsequent dose 

Warfarin is contraindicated in pregnancy as it is teratogenic

Side effects/complications of warfarin include: 
  • Haemorrhage – around 2% 
  • Alopecia 
  • Skin necrosis 
  • Purple toe syndrome 

Small print gem: warfarin possibly enhances the hypoglycaemic effect of sulphonylureas 


References

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Kearns-Sayre Syndrome

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Kearns-Sayre Syndrome is a rare disorder caused by mitochondrial DNA mutations which can result in: 
  • Ptosis 
  • Progressive external opthalmoplegia 
  • Atypical retinal pigmentation 
  • Heart block
  • Muscle weakness 
  • Ataxia 

Diagnosis is by demonstrating ragged-red fibres on muscle biopsy  


References

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Tetralogy of Fallot

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Tetralogy of Fallot is the commonest cyanotic congenital heart disease, occurring in 1 in 3600 live births. 

The four features of Tetralogy of Fallot are: 
  • Pulmonary stenosis
  • Ventricular septal defects 
  • Right ventricular hypertrophy 
  • Overriding of the aorta 

Treatment is surgical repair.

Prognosis: 
  • 40 year survival rate at least 90% 
  • Complications in adulthood include
    • pulmonary regurgitation (low-pitched, diastolic murmur) 
    • right heart failure
    • arrhythmias (6% risk of sudden cardiac death) 


References

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Vitamin C and scurvy

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Vitamin C, also known as ascorbic acid, is a vitamin found in many fruits and vegetables which plays a vital role in the formation of collagen. 

A deficiency of vitamin C causes scurvy, features of which include: 
  • Bruising
  • Fatigue 
  • Gingival hyperplasia
  • Bleeding 
  • Anaemia 
  • Bone pain 
  • Myalgia
  • Corkscrew hairs

Reasons for deficiency include 
  • Poor diet
    • Alcoholism
    • Food faddism 
    • Psychiatric illness
  • Haemodialysis (as vitamin C is not reabsorbed by the kidneys) 

Treatment is to increase vitamin C intake.


Small print gem: clinical manifestations of scurvy can be seen within 8 to 12 weeks of inadequate intake. 


References 

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Gingival hyperplasia

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Causes of gingival hyperplasia include:
  • Drug-induced
    • Phenytoin
    • Cyclosprin
    • Calcium channel blockers (nifedipine, verapamil, nimodipine) 
    • Bleomycin 
  • Hormonal surges 
    • Puberty 
    • Pregnancy 
    • Menopause 
  • Vitamin C deficiency 
  • Leukaemia 
  • Bacterial infection 
  • Hypothyroidism 


References

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Hyposplenism

/
Hyposplenism may be:

Blood film in hyposplenism may show
  • Howell-Jolly bodies 
  • Acanthocytes 
  • Target cells 

Hyposplenism results in an increased risk of life-threatening infection, particularly by:
  • Encapsulated organisms such as 
    • Pneumococci 
    • Haemophilus influenzae 
    • Meningococci 
  • Intraerythrocytic parasites 
    • Plasmodia falciparum 
    • Babesia microti

Management of hyposplenism/asplenism:
  • Vaccination
    • Pneumococcal vaccine, Hib vaccine and meningococcal B and C vaccines 
    • Yearly influenza vaccination
  • Lifelong prophylactic antibiotics should be considered with either penicillin or macrolides


Small print gem: after splenectomy, the risk of overwhelming infection is greatest in the first 2 years.

References:

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Thrombocytosis

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Thrombocytosis is a raised number of platelets, usually defined as ≥ 450 x 10^9 

Thrombocytosis may be divided into : 

  • Spurious 
    • Caused by non-platelet structures in the blood which are counted as platelets by modern automated counters 
    • Examples include 
      • Cryoglobulin crystals 
      • Microspherocytes (eg from severe burns) 
      • Schistocytes 
      • Pappenheimer bodies 
      • Bacteria

  • Primary thrombocytosis 
    • Increase in platelets caused by alterations targeting the haematopoietic cells 
    • Causes are
      • Essential thrombocytheameia 
        • Megakaryocyte proliferation 
        • Not meeting WHO criteria for CML, PV, PMF or MDS
        • Presence of JAK 2 or other clonal marker and no evidence of reactive thrombocytosis
        • Increases risk of both thrombosis and bleeding 
        • Treatment: 
          • High risk patients (aged >60 OR platelet count >1500 OR disease-related thrombotis/haemorrhage) 
            • Hydroxycarbamide plus aspirin 
            • ? interferon alpha in young patients
          • Other patients 
            • Aspirin only
      • Polycythaemia Vera
      • Myelofibrosis 
      • Chronic myeloid leukaemia

  • Secondary/reactive thrombocytosis 
    • Reactive to 
      • Infection 
      • Inflammation 
      • Post-operative/trauma 
      • Iron deficiency 
      • Hyposplenism
      • Haemorrhage 
      • Malignancy 
      • Drugs 
        • Corticosteroids 
        • Adrenaline 
    • Rarely causes complications 
    • Treat underlying cause 


Small print gem: extremely high platelet levels (>1500 x 10^9) result in more causes of bleeding than thrombosis 


References

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Wernicke’s encephalopathy

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Wernicke’s encephalopathy is a triad of: 
  • Opthalmoplegia 
  • Ataxia
  • Disturbance of consciousness and mental state 

It is caused by thiamine (vitamin B1) deficiency. 

Causes of thiamine deficiency include: 
  • Alcoholism
  • Malnutrition 
  • Recurrent vomiting 
  • Chronic diarrhoea
  • Magnesium depletion
  • Peptic ulcer disease

Treatment is IV thiamine 

Prognosis: Untreated 20% will die and 85% will develop Korsakoff syndrome



References

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HELLP syndrome

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HELLP syndrome is a complication of pregnancy, often regarded as a variation or progression of pre-eclampsia.

HELLP syndrome comprises of:
  • Haemolysis 
  • Elevated Liver enzymes 
  • Low platelets 

It complicates 10-20% of cases of severe pre-eclampsia 

HELLP occurs pre-partum in 70% of cases and post-partum in around 30%, usually within 48 hours of delivery 

Presentation tends to be
  • Epigastric pain
  • Headache 
  • Nausea and vomiting 

Treatment is delivery of baby. 

Mortality can be as high as 25%. 


References

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Pre-eclampsia

/ /
Pre-eclampsia is defined as:
  • Hypertension 
    • systolic >140mmHg or diastolic ≥ 90mmHg
    • ‘severe’ preeclampsia if systolic ≥ 170mmHg or diastolic ≥ 110mmHg 
  • Proteinuria 
  • Occurring after 20 weeks gestation 

Pre-eclampsia is a complication in 3-8% of pregnancies 
Severe pre-eclampsia occurs in 0.5% of pregnancies 

Possible features of severe pre-eclampsia include: 
  • Headaches 
  • Blurred vision 
  • Abdominal pain - epigastric 
  • Oedema
  • Clonus 
  • Liver tenderness 
  • Platelets <100 
  • Abnormal LFTs
  • HELLP syndrome

Risk factors for pre-eclampsia include: 
  • Antiphospholipid syndrome 
  • Renal disease 
  • SLE 
  • Nulliparity 
  • Chronic hypertension 
  • Diabetes 
  • Obesity 
  • Multiple gestations 
  • Advanced maternal age (> 40 years) 

Management:
  • Control blood pressure – labetalol, nifedipine or hydralazine 
  • Magnesium sulphate should be considered if eclampsia is considered a risk
  • Definitive treatment is to deliver baby 


References

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Asthma

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Asthma has a prevalence of 5.8% in the UK and is responsible for 1500 deaths annually.

Diagnosis
  • Features that increase the probability of asthma: 
    • Wheeze, breathlessness and cough, particularly if 
      • Worse at night/early morning
      • Occur in response to exercise, allergens, cold air, aspirin or beta blockers 
    • Family or personal history of atopy 
    • Widespread wheeze on auscultation 
    • Otherwise unexplained low FEV1 or PEF 
    • Otherwise unexplained peripheral blood eosinophilia
  • Features that lower the probability of asthma:
    • Prominent dizziness/light-headedness
    • Chronic productive cough in absence of wheeze or breathlessness 
    • Voice disturbance 
    • Significant smoking history

Management

  • If high probability of asthma – trial of treatment 
  • If intermediate probability – perform spirometry
    • FEV1/FVC <0.7 – trial of treatment 
    • FEV1/FVC >0.7 - consider referral to specialist 
  • Low probability – consider referral to specialist 

An increase of PEF >15% from baseline or increase of FEV1 > 400mls following a trial of treatment supports the diagnosis of asthma 


Treatment

Chronic asthma
  • Step 1: 
    • Inhaled short-acting beta 1 agonist PRN 
  • Step 2: 
    • Step 1 + inhaled steroid 
  • Step 3: 
    • Step 2 + long-acting beta 2 agonist 
    • If control still inadequate consider 
      • Stopping long-acting beta 2 agonist if no response
      • Increasing inhaled steroid 
      • Trial of leukotriene receptor antagonist or SR theophylline
  • Step 4: 
    • Step 3 + Further increase of inhaled steroid 
    • Addition of leukotriene receptor antagonist or SR theophylline or beta 2 agonist tablet
  • Step 5: 
    • Step 4 + oral steroid 

Acute asthma attacks 

  • Assement of severity of asthma 
    • Acute severe
      • Any one of
        • PEF 33-50% best or predicted 
        • Respiration rate ≥ 25/minute 
        • Heart rate ≥ 110/minute 
        • Inability to complete sentences in one breath 
    • Life-threatening
      • Any one of 
        • PEF <33% best or predicted
        • SpO2 < 92%
        • PaO2 < 8 kPa 
        • Normal PaCO2
        • Silent chest 
        • Cyanosis
        • Poor respiratory effort 
        • Arrhythmia 
        • Exhaustion, altered conscious level
    • Near fatal 
      • Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures 

  • Treatment of acute severe asthma 
    • Oxygen 
    • Nebulised salbutamol 
    • Nebulised ipratropium bromide 
    • Prednisolone 40-50mg od – continue for at least 5 days or until recovery 
    • Consider single dose of IV magnesium sulphate 

  • Admit patients: 
    • With any feature of life threatening or near fatal attack 
    • Any feature of severe attack persisting after initial treatment
    • Patients whose peak flow is >75% predicted or best one hour after initial treatment may be discharged from ED unless there are other indications for admission 

  • If patient is admitted, prior to discharge patient should: 
    • Have been on discharge medication for 12-24 hours
    • Have PEF >75% predicted or best and PEF diurnal variability <25% 
    • GP follow up arranged within 2 working days 
    • Respiratory clinic follow up within 4 weeks 


Small print gem: female gender is a risk factor for persistence of asthma from childhood to adulthood.


References:

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Erythema nodusum

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Erythema nodusum, the commonest panniculitis, is characterised by painful, tender erythematous nodules most commonly located on the shins. 

There may be a prodomal illness of malaise, low-grade fever, cough and arthralgia prior to the appearance of nodules. 

It tends to heal without scars. 

Causes of erythema nodosum include: 
  • Infections 
    • Streptococcal – most commonly identifiable cause 
    • Mycoplasma 
    • Mycobacterium  (TB) 
    • Yersinia
    • Chlamydia 
    • Viral infections 
  • Drugs 
    • OCP 
    • Antibiotics 
    • Plus many more 
  • Other 

Management
  • Treat underlying condition 
  • NSAIDs for pain 


References

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Extrinsic allergic alveolitis

/ / /
Extrinsic allergic alveolitis, AKA hypersensitivity pneumonitis, is a group of immune-mediated lung diseases in which repeated inhalation of allergens results in type III and type IV hypersensitivity reactions with granulomatous inflammation. 

Most cases take years of repeated exposure to the allergen before EAA develops; once it does, symptoms tend to occur 4 to 8 hours after inhalation of an allergen: 
  • Dyspnoea 
  • Unproductive cough 
  • Fever 
  • Myalgia

Chronically patients have permanent dyspnoea, emphysema, pulmonary fibrosis and weight loss, with the potential to progress to respiratory failure and cor pulmonale. 

Forms of extrinsic allergic alveolitis include: 
  • Farmer’s lung – thermophilic actinomycetes, Saccharopolyspora rectivirgula (Micropolyspora faeni), and Aspergillus umbrosi 
  • Bird fancier lung 
  • Malt worker’s lung – aspergillus species
  • Hot tub lung - mycobacterium avium complex
  • Japanese summer disease – various fungi from moldy houses – t. cutaneum

Investigations 
  • CXR – pulmonary infiltrates; fibrosis upper lobes > lower lobes
  • HRCT – ground glass shadowing, gas trapping
  • Lung function tests: 
    • Spirometry – restrictive pattern
    • Diffusing capacity for carbon monoxide – decreased 
  • Bronchial lavage – initially neutrophils then lymphocytes

Management 
  • Avoidance of allergen
  • ?steroids

References

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Steven-Johnson Syndrome and Toxic Epidermal Necrolysis

/ /
Steven-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are both severe cutaneous adverse reactions, characterised by target lesions, blistering and mucosal involvement. 

The difference between SJS and TEN is the extent of body surface involvement: 
  • SJS <10% of body surface involved 
  • TEN >30% 
  • Between 10% and 30% is SJS/TEN overlap

Patients are systemically unwell. 
Nikolsky’s sign is positive (mechanical pressure on skin causes epidermal detachment) 

Causes of SJS/TENS: 
  • Medications
    • Antibiotics 
      • Sulfonamides 
      • Trimethoprim 
      • Penicillin 
      • Cephalosporins 
      • Quinolones 
    • Antiepileptics 
      • Carbamazepine 
      • Lamotrigine 
      • Phenytoin 
    • Other 
      • NSAIDs 
      • Allopurinol 
  • Infections 
    • Mycoplasma pneumonia 
    • Herpes simplex 

Median time from starting drug to symptoms is under 4 weeks 

Treatment 
  • Stop any causative drug 
  • Supportive treatment 
  • IV IG 

Prognosis
Approximately 10% mortality for SJS, 30% for overlap and 50% for TEN 


References

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Acute altitude illness

/ / / / / / /
Acute altitude illness encompasses  acute mountain sickness, high altitude pulmonary oedema and high altitude cerebral oedema.


1) Acute mountain sickness (AMS)

Acute mountain sickness is generally a self-limiting condition that occurs at altitudes >2500m. It develops gradually over 6 to 24 hours. 

Features include: 
  • Headache 
    • Worse on moving/lying down
    • Improves after vomiting 
  • Vomiting
  • Dizziness
  • Fatigue 
  • Insomnia 
  • Anorexia 

Fitter, younger individuals tend to suffer from AMS most. 

Prevention:
  • Gain height at no more than 500m per day 
  • Medications:
    • ?Acetazolamide (carbonic anhydrase inhibitor) 
      • Risk of Stevens-Johnson syndrome, renal failure and toxic epidermal necrolysis 
    • ?sidenafil/tadalafil  

Treatment: 
  • Descent
  • Oxygen 
  • ?Acetazolamide
  • ?Dexamethasone


2) High-altitude pulmonary oedema (HAPE)

Presents like pulmonary oedema 

Treatment
  • Descent 
  • Oxygen 
  • Acetazolamide 
  • Dexamethasone 
  • Nifedipine 
  • Sildenafil/tadalafil 


3) High-altitude cerebral oedema (HACE) 

Presentation includes ataxia, confusion, altered mental status and papilloedema. 

Treatment
  • Descent 
  • Oxygen 
  • Dexamethasone 
  • Acetazolamide 


References:

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Secret collector of interesting anonymised ECGs. Fan of the Bath Photomarathon. Lover of cream teas. [Sarah Hudson] (Your Picture)