Digoxin toxicity presentations

I came across a patient few days ago, 80 year old M with CCF on digoxin presented with an episode of sudden onset of dizziness lasting for around 3-4 minutes. The patient worried about digoxin toxicity. I used this opportunity to remind myself on the signs and symptoms of digoxin toxicity.

We can divide digoxin toxicity into acute or chronic:

Acute:
- GI: anorexin, vomiting, nausea, diarrhoea and abdominal pain
- Metabolic: hyperkalaemia (early sign of significant toxicity)
- CNS: enhanced automaticity with AV block, VF, VT, ventricular ectopic beats, bradyarrhythmias, hypotension and shock
- CNS: lethargy and confusion

Chronic digoxin toxicity:

Other features of chronic toxicity commonly described in textbooks are visual disturbances (e.g. reduce acuity, yellow halos (xanthopsia) and altered color perception (chromatopsia)}

Reference:

http://lifeinthefastlane.com/ccc/digoxin-toxicity/

Hepatitis B serology interpretation

I have struggled with Hepatitis B serology interpretation for a long time. I am trying to learn it properly for the exam, and also it is a common infection. In Australia, around 1 % of the population has Hepatitis B.

Key point:

- We are testing for 2 things here. One is antibody and one is antigen.

- Diagnostic test: To diagnose Hepatitis B. Only need to order 3 tests.

1. Hepatitis B surface Antigen: The presence of Hepatitis B surface antigen indicates infection.
2. Hepatitis B core antibody: The presence of antibodies to Hepatitis B core antibody indicates past infection or current infection. 
3. Hepatitis B surface antibody: present after vaccination and resolved infection.

- The following is a table which summarises the interpretation of the test results:

- How I remember this is that I remember HbsAg as a thief, anti-HBc as a security guard and anti-HBs as the policeman. HBsAg means the thief is in the shop and it means infection. When the thief is caught by the security guard (anti-HBc), the problem is still not solved completely until the policeman arrives (anti-HBs). If the policeman is there (anti HBs), no thief will come in and indicates immunity.

- Markers of hepatitis B virus infection : HBV antigens and host antibodies, HBV DNA and genotype, biochemical markers, and the degree of hepatic fibrosis and inflammation. 

- HBeAg: it promotes persistent infection 

- Antibody to e-antigen: not a protective antibody but its presence indicates better immunological control.

- HBV DNA

- ALT: indications for liver damage. Recent studies have shown that normal range of ALTs are <30 in men and < 19 in women 

- The following picture summarises the 4 phases to treatment decisions

- Immune tolerance: The immune tolerance phase is characterised by hepatitis B e antigen (HBeAg) positivity, high HBV DNA levels (>20,000 IU/mL, and commonly over 1 million IU/mL), normal ALT levels and minimal level liver injury. During this phase, which may persist for decades, liver inflammation or fibrosis is either absent or minimal. This phase is associated with a low risk of progression to advanced liver disease, and it is thought to occur most commonly in those who acquire the infection vertically from HBeAg-positive mothers. 

- Immune clearance phase: the immune clearance phase is also called the immune competent or active phase. The liver injury in HBV is determined by the immune response to the virus. The host's immune system recognises the HBV as foreign, and mounts a cytotoxic response to infected hepatocytes. This phase is characterised by fluctuating HBV DNA and ALT levels. Recurrent bouts of active inflammation and , eventually, fibrosis can occur int he liver following these repeated immune 

Mediated attacks. An important outcome of this phase is the seroconversion of HBeAg to anti-heb, which is associated with a lower level of viraemia. The observed rate of clearance of HBeAg in those with or without elevated ALT levels averages 8%-12% per year. However, a number of people will still develop active liver disease after HBeAg seroconversion, generally owing to immune escpape; that is, emergency of HBV mutant variants, particularly the core or preacher mutation that renders the virus unable to encode for HBeAg.

Reference:

Hepatitis B for GP

H. Pylori

H. Pylori 

Key features: 

1. H. pylori is a gram negative bacillus that has naturally colonised the human stomach for at least 50,000 years. Usually acquired in childhood, it colonises the gastric mucosa of about 50% of the world’s population at some time in their life. 
2. Infection with H. pylori induces a persistent immune response. Because the organism has numerous adaptions to prevent immune detection, clearance by the body is never complete. The resulting sustained inflammatory processes in the stomach cause a reduction in the population of somatostatin-producing D cells. This causes a subsequent rise in gastrin secretion followed by an increase in gastric acid release which may lead to peptic ulceration in some patients. 
3. Most patients colonised with H. Pylori do not develop peptic ulcers. 
4. It would not be appropriate to investigate for H. pylori initially in the presence of alarm symptoms such as weight loss, bleeding, dysphagia or symptoms in a patient above the age of 55 years. In this context, investigations should first be directed at excluding malignancy, for example with a gastroscopy.
5. Current Therapeutic Guidelines in Australia, revised in July 2013, recommend PPI-based triple therapy as the first line measure for eradication of H.pylori. (Esomeprazole 20 mg twice daily, amoxicillin 1 g twice daily and clarithromycin 500 mg twice daily)
6. The conclusion to be drawn from the Swedish study is that in all traditionally prescribed regimens, eradication is only partially successful. 

Reference:

http://www.racgp.org.au/afp/2014/may/helicobacter-pylori-eradication/

Gout

Gout

Key points:

1. Gout is the most common inflammatory arthritis with a prevalence of about 2% in Australasia.
2. Key steps in the development of gout are 1)chronic hyperuricemia 2) monosodium rate monohydrate 3)interaction between the crystals and the inflammatory system, which is primarily responsible for the clinical features. 
3. Definition of hyperuricemia: serum rate level > 0.42
4. Hyperuricemia is caused by medications and genetic predisposition
5. Only 20% of patients with hyperuricemia develop gout 
6. Definite diagnosis can only be achieved via synovial fluid analysis. This needs to be done before recommending hypouricemic drug therapy.
7. Management of acute gout:
1. 
8. There is an increase risk of gout when the patient is started on rate lowering therapy. Patients can be started on low dose colchicine 0.5 mg daily or daily NSAID or 5mg prednisolone. Usually prophylaxis is required for around 3-6 months.
9. Serum rate target is less than 0.36 mmol/L, however for patients with a large rate crystal load (as reflected by the presence of tophi) erosions or chronic joint deformity due to gout, the target is a serum rate of less than 0.3 mol/L/
10. Diet and lifestyle modification alone usually is inadequate to lower serum urate level.
11. Allopurinal hypersensitivity syndrome occurs with greater frequency in the setting of renal insufficiency, advanced age, HLA B58:01 positivity and higher initial doses but can occur in their absence. The syndrome usually occurs in the first 12 weeks of exposure, and thus the development of rash during this period should prompt immediate cessation of allopurinol, assessment of liver and renal function, and for the possibility of hypersensitivity. 
12. Probenecid is another agent which can be used as rate lowering agent. But the patient needs to have renal function > 30-40ml/min. Because of the marked increase in urinary uric acid in the early phase of treatment, good hydration and urinary alkalisation are appropriate. 

REST Course key points

REST COURSE 

I attended the REST (Rural emergency skills training) course over the weekend. It is decided for doctors who are not emergency physicians and want to have a structured approach to an emergency situation. 

Some key points I got from the course:

1. Use DRSABCD in all emergency situations. Write down this on a white board and try to be prepared as much as you can. 
1. D: Danger 
2. R: Response (AVPU) Response to pain = PU = may require intubation 
3. S: send for help! or SHAVE = Sugar, haemorrhage, adrenaline, VT/VF and Epilepsy
4. A: Airway + Cervical spine 
5. B: Breathing, Oxygen, Pulse oximeter, RR, Ausculation 
6. C: Circulation. Blood pressure, HR, Cap Refill, IV access
7. D: Disability. Pupil and spine 
2. Must know adrenaline dose 
1. only use IV adrenaline in someone who is dead 
2. Anaphylaxis: adult 0.5 ml in 1:1000
3. Anaphylaxis: paediatric 0.1ml/kg in 1: 10,000
4. Arrest: adult 1 ml in 1:1000
5. Arrest: paediatric 0.1 ml/kg in 10,000
3. Protecting the cervical spine is important. When in doubt, put the cervical spine collar on. 
4. Defibrillation: 200 J. Use it early in VT/VF
5. Protecting the airway is important but it doesn’t always require intubation to improve breathing. Try guedel or LMA. 
6. Fluid bolus formula is 20mg/kg
7. Paediatric weight calculation for 1 year or above (age +4) x 2 
8. Don’t forget to check sugar 
9. intraosseous can be placed medial to tibial tuberosity 1 cm below the articular surface
10. Don’t forget the 4Hs and 4Ts. Haemorrhage, hypoxia, Hypokalaemia/hyperkalaemia, Hypothermia. Tension pneumothorax, Tamponade, Toxins, Thrombosis