an obscure acidosis…

The Case.

64 year old male attends your ED with a complaint for 3 months of progressive weakness, however over the past 7 days he has had multiples falls secondary to his ‘legs just completely giving way’.  You note on the hospital records that he has a history of alcoholism (150-250 grams per day). After a long & drawn out discussion (think, blood from a stone) in an attempt to elaborate his history, you gain the knowledge that …

  1. he has had some chronic worsening, low back pain
  2. he has not eaten a proper meal for over a week (and no alcohol in that time either)
  3. he has lost a ‘decent amount of weight’, but cannot objectify it any further.

He has no known past medical history & takes no regular medications.

He looks crook. Pale, diaphoretic and clammy. Tachycardic (@120/min) and hypertensive (165/110 mmHg). He is afebrile however. No murmurs, chest clear. Tender hepatomegaly. No midline back pain. Normal power, sensation and reflexes to both legs (with good peripheral pulses).

Here is his venous blood gas and accompanying chemistry….

VBG01

What are your thoughts ?
Differential diagnoses ??
What are you going to do next ???

My Interpretation.

  • Metabolic acidosis with respiratory compensation
    • HAGMA
    • Expected CO2 = 29 ± 2 mmHg
      • Actual CO2 = 24, therefore concomitant Respiratory Alkalosis.
  • Lactic Acidosis ?cause
    • ?Sepsis (source unclear)
    • Osmolar Gap = normal.
    • Paracetamol / Salicylates / Ethanol = negative.
    • Medications / Drugs unlikely (he’s not taking any).

This fella was covered with broad spectrum antibiotics, given reasonable volumes of crystalloid and loaded with thiamine. His CXR, urine, CT-Abdomen (with spinal reconstruction) and CT-Brain were all unremarkable, so was admitted as a lactic acidosis (cause unknown), presumptive sepsis (source unclear) and likely alcoholic liver disease (low PLTs, tender RUQ). Click HERE to see his gradually resolving lactate (over the course of 6-7 litres of fluid).

Lactic Acidosis.

The Brief Biochemistry.

Lactic acid is derived from the metabolism of pyruvic acid (catalysed by lactate dehydrogenase & involving NADH & NAD+). Lactic acid is rapidly buffered (by extracellular HCO3) resulting in the generation of lactate. Lactate itself is metabolised back to pyruvate (largely by the liver, and a little by the kidney), which is then converted to CO2 & water or glucose.

The Types & Causes.

Type A.

    • Associated with clinical evidence of poor tissue perfusion or oxygenation of blood (eg. hypotension, hypovolaemia, hypoxaemia, cardiac failure or sepsis).
    • Overproduction.
        • Sepsis, sepsis, sepsis…
    • Underutilisation:
        • Liver disease
        • Inhibition of gluconeogenesis
        • Thiamine deficiency
        • Uncoupled oxidative phosphorylation.

Type B.

    • No clinical evidence of hypoperfusion.
    • Three subtypes.
        • B1 = associated with systemic disease
              • Renal & hepatic failure
              • Diabetes
              • Malignancy
        • B2 = drugs & toxins
              • Metformin
              • Alcohols
              • Iron
              • Isoniazid
              • Salicylates
        • B3 = inborn errors of metabolism.

Personally, I find Cliff Reid’s LACTATES mnemonic much more helpful ….

L = Liver & Lung disease
A = Accelerated Glycolysis (adrenaline, salbutamol)
C = Congenital Disorders
T = Thiamine Deficiency
A = Anaerobic Metabolism
T = Toxic & Drug Effects 
E = Extracellular Movement in Alkalosis
S = Sepsis

* http://resusme.em.extrememember.com/some-causes-of-a-raised-lactate/
So, what happened next…..

The Finale.

The follow morning, the Haematology Registrar calls the admitting team after looking at his blood film.

Blood Film

He proceeded to Bone Marrow Biopsy that afternoon which confirmed the presence of Burkitt’s Lymphoma.Interestingly, this has been (rarely) linked to unexplained lactic acidosis in several case reports (here & here). Whilst the pathogenesis of the lactic acidosis in leukemia, lymphoma, and solid malignancies is unclear, it has been suggested that either direct lactate production by the neoplastic cells or associated thiamine or riboflavin deficiency may play a role.
References.
  1. eMedicine – Lactic Acidosis 
  2. Resus.me – Some Causes of Raised Lactate
  3. UpToDate.com – Causes of lactic acidosis
  4. Reid C, Rees V, Collyer-Merritt H. Non-septic hyperlactataemia in the emergency department. Emerg Med J. 2010 May;27(5):411-2.
  5. Glasheen JJ, Sorensen MD. Burkitt’s lymphoma presenting with lactic acidosis and hypoglycemia – a case presentation. Leuk Lymphoma. 2005 Feb;46(2):281-3.

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