Potassium

Axioms: K is abundant in all cells (~50mmol/kg body weight, ~3500mmol K adults), and is found in a much lower concentration in plasma. Acidaemia shifts K+ out of cells, Alkalaemia shifts K into cells. Cells also absorb K when they absorb glucose. Aldosterone causes Na retention and K excretion. K normal range is 3.5-5.0 mmol/l. Every 0.5 over/under means a ~150mmol extra/deficit. Hyper/Hypo's cause parasthesias and weakness.

• Hypokalaemic Patients: Cramps and apathy. ECG showing Saggy ST, Depressed T. Think urinary or GIT losses. Diuretics, NVD, laxitives and such. Eating too little? Anorexia. Remember aldosterone from the RAS system makes the body keep Na, in exchange for losing K. So hyperaldosteronism or mineralocorticoid excess causes it too. Consider axioms; insulin excess (eg after glucose load) will shift K into cells.

• Hyperkalaemic Patients: Hypotensive and bradycardic. ECG showing depressed P, peaked T (look for these in all ECGs as it is not well autodetected). Think renal failure, especially if older. Remember cells contain lots of K, so think about haemolysis, rhabdomyolysis, and tissue damage. Insulin deficiency means K accumulates in blood, causing mild hyperkalaemia. Drugs drugs drugs; NSAIDS, K sparing diuretics (spironolactone, amilioride), drugs that dampen the renin-angiotensin-aldosterone system (ACEi, ARBs. see axiom on aldo)

Low K Approach
Chlorvescent has 28mmol K per dose. SlowK has 600mg or 8mmol K. Infusion over 40mmol/L cannot be done peripherally. Infusion over 10mmol/hr is dangerous. Typical IV dose is 30mmol K over 6/24 (5mmol/hr), with 2/24 monitoring.

1. Slow release potassium. Target 16mmol per day. eg. 1 x SlowK (8mmol) BD
   
2. If severe: 10mmol/100ml premix infused 3/24.
3. Maintain with spironolactone 50mg po BD
   

High K General Approach:

• ALWAYS stabilize myocardium if severe: calcium gluconate 10% 10ml *large vein, slow 5min push.
• If severe: 10units Actrapid iv bolus + 50ml 50% Glucose over 5min. CI hypoaldosteronaemia as it precipitates refractory hypoglycaemia.
  
• If very severe: Consider dialysis. Short term salbutamol 0.5mg iv stat.
  
• Moderate: Sodium Polystyrene Sulfonate 15g po tid
  
• If applicable: Rehydrate patient to restore renal function. Consider Furosemide.
  
• Review meds.

High K + Chronic Renal Failure: As above. Review meds.

High K + Severe Metabolic Acidosis w Volume Depletion: Start with 50ml Sodium Bicarb 1mmol/mL iv over 10min w ECG monitoring. Repeat every hr as necessary. Aim to restore normal hydration.

High K + Adrenal Insufficiency: Seen in some CRF patients. Normal glucocorticoids but aldo deficient. Sole Mx if not acute is fludrocortisone 150mcg po sid.

Sepsis: Approach and Empiric Tx

End-organ-damage OR hypotension, PLUS fever, tachycardia, tachypnoea, WCC++

Overall Approach
1. CULTURES first. Two bloods. Urine, sputum, wounds as appropriate.
2. Antibiotics
3. Start fluid resus. NS 300ml iv bolus if poor peripheral circulation, confusion, oliguria OR lactate>4mmol/l.
4. Correct Hypotension with target >90/65. Fluid resus then consider Noradrenaline or dopamine infusion.
5. Maintain O2 and glucose.
6. Consider corticosteroids if unresponsive to fluids and vasopressors.
7. Tx according to culture results and choose abx appropriately.
8. If fever persists for >4 days, seek ID Consultant.

Unknown source.
Adults: Flucloxacillin 2g iv qid + Gentamicin 7mg/kg iv stat.
Febrile, Neutropenic: Piperacillin+Tazobactam 4+0.5g iv tid (Tazosin). Add vancomycin if in shock, has MRSA, or high MRSA incidence in ward.

Child, Meningitis Not Excluded (Playing it very safe!)
Over 6 months, Cefotaxime 50mg/kg iv qid.
Under 6 months, add Amoxycillin 50mg/kg iv qid PLUS Vancomycin 30mg/kg iv bd infused.

GIT source?
Metronidazole 500mg iv bd, Amoxicillin 1g iv qid, Gentamicin 6mg/kg*.
Beyond 3 days, stop all above, use Piperacillin+Tazobactam 4+0.5g iv tid (Tazosin).

Intravascular Device?
Flucloxacillin 2g iv qid PLUS Gentamicin 7mg/kg*
MRSA likely, replace fluclox with Vancomycin 1.5g iv bd inf.


*see post on gentamicin dosing.

Urinary Tract Infections

Other than mild cystitis, MSU culture before starting abx if possible. Consider blood cultures if pyrexic and unwell with NV (suspect sepsis). In men, consider urology review (congenital malformations) if recurrent. Nitrates in urine has a very poor sensitivity (<50%). Consider risk of trimethoprim in women of childbearing age! Cranberry products reduce symptoms but do not resolve UTI!

Cystitis: Dysuria, Polyuria, Urgency, Nocturia, Cloudy, Urine, WBC & RBC.

• .Trimethoprim 300mg po sid 3/7.
• If pregnant, or Trimethoprim doesnt work, use Cephalexin 500mg po sid 5/7.
• Resistant to all, then Norfloxacin 400mg po BD 3/7.

Pyelonephritis: NV, 38C+, abdo/flank pain, white cells, MCS+.
For mild cases (low fever, no sepsis, no vomiting), treat as per cystitis - trimethoprim then norfloxacin. If septic, give Gentamicin 6mg/kg iv stat PLUS Amoxycillin 2g iv qid. Repeat in 24h if eGFR > 60. If low eGFR, liase ID reg. Max 3 doses genta.

Recurrent UTI: Tx as per pyelonephritis.

• Women: Trimethoprim 150mg po nocte up to 6/12 as prophylaxis; review if still recurrent. Consider pre-intercourse stat doses. Consider self administer trimethoprim 300mg 3/7 regime, with instructions to seek help when not resolved in 2/7.
• Men: Consider prostatitis if symptoms include lower back / perineal pain, painful ejaculation. Ix DRE prostate.

Warfarin, The Bottom Line.

Warfarin is a Vitamin K antagonist. It can be reversed by administering Vitamin K but takes around 24hours as clotting factors need to be replenished.

Causes hypercoagulable state in the first 36h of use by decreasing protein C levels - NOT suitable for VTE prophylaxis for short term inpatients. Warfarin takes around 72h to take effect.

• Target INR 2.0. Start to worry when INR > 4. Consider skipping next dose and reducing the warfarin prescription.
• When INR > 9 without bleeding; Vit K 2.0mg po stat. Stop warfarin and watch until INR therapeautic. Restart on lower maintenance dose.
• Significant bleeds? Regardless of INR, start Vit K 10mg IV over 30min, then three units of fresh frozen plasma, consider 20mcg/kg Factor VIIa bolus over 5 min.

CHADS Score

In patients with Atrial Fibrillation:

Congestive Heart Failure 1
Hypertension 1
Age > 75 1
Diabetes 1
Stroke/TIA 2

Score of 1: Start on Asprin.
Score of 2: Warfarin, with target INR2.0-3.0

A Practical Approach To Blood Gasses (Acid Base Disorders)

Many textbooks and online resources contain too much information as the physiology of blood gasses is scarily complex (the exact physiology of metabolic alkalosis is still poorly understood). Thankfully, it's not nearly as difficult in clinical practice. Here is a method of interpreting blood gas (ABG/VBG) results; sans minutiae; with an easy-to-understand logical approach focusing on distilled, clinically-relevant axioms.

pH 7.35-7.45
CO2 35-45 mmHg
HCO3 22-30mmol/l
Anion Gap 15
Base Excess -3 to +3

1) Is it acidaemia (<7.35) or alkalaemia (>7.45)?
Acidosis is a pathological process causing the blood to become more acidic. You can have an acidosis and alkalosis simultaneously and have a normal pH. Hence the terms acidaemia and alkalaemia are more suitable.

2) Is it metabolic or respiratory in origin?
CO2 = acid, generally respiratory in origin.
HCO3 = base, generally metabolic in origin.
Acidaemia can be either caused by low HCO3 or high CO2. Inversely, alkalaemia can either be caused by high HCO3 or low CO2.

3) Are there excess organic acids? Check the Anion Gap! Na+K-Cl-HCO3
This figure tells you if there is extra acid, loss of bicarbonate, or both. Note that albumin is an anion that contributes significantly to the normal AG of 15. Hypoalbuminaemia causes the AG to be skewed lower. Infusing a patient with HCl will not increase the AG! Organic acids have anions that bind to HCO3 but the anions themselves are not counted in the equation. That's why the AG is useful. If AG>30, metabolic acidosis is present fullstop.

4) Just losing HCO3, without any excess organic acids (normal AG)?
GIT secretions are generally rich in HCO3, and diarrhea will cause the kidneys to compensate by adsorbing more Cl. In renal tubular acidosis, the kidneys dont readsorb enough HCO3 and retains too much Cl.

4) Look at the base excess (+-3) for severity of the metabolic disturbance.
This is simply the amount of acid (base if negative) required to bring the pH back to 7.4 in vitro, independent of pCO2.
BE +5 suggests mild metabolic alkalosis.
BE -12 suggests severe metabolic acidosis.

5) A simple way to look at compensation
Respiratory disturbances will change pCO2 (away from pCO2=40). The body uses HCO3 as a buffer, and hence HCO3 will rise/fall to counteract the gain/loss of CO2. 1425AcidBase. Remember...1.4.2.5.Acid.Base. In the chronic setting the body logically has more time to increase the HCO3 concentration so the second number is for chronic while the first is for acute.

• Acidosis: Every 10 pCO2 up, 1 or 4 HCO3 up.
  
• Alkalosis: Every 10 pCO2 down, 2 or 5 HCO3 down.

Metabolic disturbances on the other hand tend to be compensated by changing the pCO2. The rule of thumb for the change in pCO2 is even simpler to remember.

• The last two numbers of pH. eg. pH7.30, expect pCO2=30

In Practice:

Watch out for FALLING BICARBONATE / TACHYPNOEA in all patients
Because metabolic acidosis cannot be ignored. Do ABGs/VBGs. if pCO2 is not elevated...and HCO3 is low, then there is a metabolic acidosis.

• High AG (organic acids present): Left - Lactate; Total - Toxins (salicylates); Knee - Ketones; Replacement - Renal Failure
  
• Low Look at the AG equation. A metabolic acidosis (read: drop in HCO3) with a normal anion gap can only exist if Cl goes up. Thats why a normal AG metabolic acidosis is also known as a hyperchloremic metabolic acidosis. Think diarrhoea and RTA.
  

Credits:
This article is loosely based on a lecture (Approach to Acid-Base Disorders) by Dr Tim Crozier at Maroondah Hospital, Ringwood, VIC Australia.

Notes: Anticoagulants

unsorted axioms...

• In pt w valve replacements, use anticoagulants regardless even for bowel scopes. Reverse warfarin with Vitamin K then cover with easily reversible LMWH (Clexane).
• Pt w Mitral Valve pathology at especially high risk of clots due to low flow at mitral valve.