Download Week 2 File - ACI Moodle

EMERGENCY MEDICINE
Liverpool Hospital
The Weekly Probe
3rd February 2014
Volume 17 Issue 2
Welcomes and Farewells- As the end of the term approaches there are new staff arriving and
others moving to ?greener pastures. Thanks to all those moving on for all your hard work over the
term, and for some of the regs, over the years. Thanks again.
For the new staff, welcome. The place may seem a bit daunting at times but there is always someone
to ask for advice and support.
Rabies – occasionally we get visitors from overseas with recent potential exposure and non-travellers
who may have been exposed to lyssavirus carried by bats. The info on this has been placed on the
intranet site under “Clinical” then “medical” then "Infectious Diseases". Notify the Public Health Unit –
they will also help organise the deliver and administration of the immunoglobulin and vaccine.
Up-to-date – you may have tried to access Up-to-date unsuccessfully this week but the Hospital
subscription is not being renewed- bugger! An option is Dynamed which is evidence based and more
in point form. For access go to the Hospital web site then Libraries on the right then Liverpool – the
link is on the right bottom of the screen. The advantage of this new service is that it is designed for
point of care access with point form and you can get free access on you smart phone or ipad etc – go
to Athens link on the left hand side http://www.swslhd.nsw.gov.au/liverpool/library/ then to the
Athens registration form. Less detailed and to be honest it’s a bit of a step down from up-to-date.
Urine microscopy- After discussions with micro over the last week, it has been pointed out that urine
samples are assessed on a automated IRIS instrument. Apparently this is fast, accurate and reliable
and we have substantially reduced the time to reporting of routine urine microscopy as a result.
However they don’t report routinely on the presence or absence of bacteria. However if you clinically
feel that this would change your management ring the lab and ask if this can be reported.
Andi’s Trek – Andi Rauch has entered the Coastrek team challenge, a 50km walk to raise funds for
The Fred Hollows Foundation, a charity which does a great job world-wide. Go to
https://secure.coastrekfundraising.com.au/registrant/PersonalPage.aspx?eventid=43849&Registratio
nID=672065 to help a great cause.
THIS WEEK
Alcoholic ketoacidosis
Metabolic acidosis
Ketone meter
Next Week
Joke / Quote of the Week
The Week Ahead
Alcoholic ketoacidosis:
54yo man with Hx of previous alcohol abuse presents with abdo pain post binge. No vomiting. Lipase
292 pH 7.1 Co2 24 , bicarb 9 BE -17 lactate 1 - EUC Na 132/ K 4.2 / Cl 98 /bicarb 9/ Urea 3.2 / Cr
71 BSL 6
What is it and how do we treat?
Similar to other conditions in the ED our first priority is the ABCDEs, analgesia and supportive
management. Looking at the various pathologies we need to treat precipitating factors and
complications in this case the pancreatitis. However looking at the above VBG we note the pH of 7.1
and the CO2 of 24 which is consistent with a partially compensated metabolic acidosis.
Metabolic Acidosis
When you find a patient with an acidosis the first thing to do is calculate the anion gap so you can
place the acidosis in a category of either normal anion gap & high anion gap acidosis.
Anion gap = Na + K - (Cl + HCO3).
Normal = 15 +/- 2,. The anion gap is due to sulphates, phosphate, protein, especially albumin,
organic acids eg. lactic acid.
In this case the AG was 132 + 4.2 – (98+9) = 29.2 – thus elevated AG.
Increased anion gap acidosis can be due to:
 increased anion production (DKA, lactic acidosis, starvation, alcoholic ketoacidosis, inborn
errors) or
 ingestion of toxins (salicylate OD, paraldehyde, methanol, ethylene glycol, cyanide, isoniazid,
toluene), or
 acute/chronic renal failure.
There are some great pneumonics to help you remember the causes of the acidosis.
DULSI (like the old women’s name) is the easiest – Diabetes, Uraemia, Lactic acidosis, Salicylates
, Intoxicants
Increased Anion Gap acidosis: MUDSLEEP. Methanol, Uraemia, DKA, Salicylate, Lactate,
Ethanol, Ethylene glycol, Paraldehyde + cyanide, + inborn errors of metabolism, + iron, isoniazid.
Some people use the pneumonic MUDSLIDE to help them remember.
Also consider the Osmolar Gap.
Normal serum osmolality 280-300.
Calculated serum osmolality = (2xNa) + Glucose + Urea.
Osmolar Gap = Measured - Calculated. An osmolar gap > 10 is significant & indicates the
presence of osmotically active substances eg. ethanol, methanol, ethylene glycol, isopropyl
alcohol, mannitol.
Normal Anion Gap acidosis can be due to:
 GIT loss of HCO3 (diarrhoea, ureterosigmoidostomy, anion-exchange resin, small bowel
drainage, Ca Cl2, Mg Cl2., or
 Renal loss of HCO3 (carbonic anhydrase inhibitors, renal tubular acidosis,
hyperparathyroidism, hypoaldosteronism), or other (dilutional acidosis, hyperalimentation
acidosis, sulphur ingestion, HCl ingestion).
Can use the pneumonic USED CARP. Ureteroenterostomy / obstructive uropathy, Small bowel
fistula, Extra Cl, Diarrhoea, Carbonic anhydrase inhibitors, Addisons, Renal tubular acidosis,
Pancreatic fistula.
Low anion gap acidosis: can be due to Lithium toxicity (increased unmeasured cation), multiple
myeloma (increased positive charge of abnormal proteins), hypercalcaemia, hyperMg, bromide
intoxication.
Lactic Acidosis can be divided into Type A or Type B.
Type A: due to poor perfusion with tissue hypoxia eg. severe hypoxia, severe anaemia,
haemorrhage, CCF, CO/CN poisoning, generalised seizures.
Type B is where tissue hypoxia is not apparent such as in diabetes mellitus, Renal & liver failure,
malignancy such as lymphoma, leukaemia or sarcoma, & drug ingestion such as ethanol, methanol
& biguanides, salicylates, isoniazid, fructose, sorbitol; & congenital enz deficiencies (G6Pase defic).
Editor: Peter Wyllie
Compensated metabolic acidosis – the body will try to compensate when the pH reduces through
the loss of exhaled CO2 - As useful rule in metabolic acidosis – the P aCO2 should equal the last 2
digits of the pH. However note you can get 2 pathologies occurring simultaneously – respiratory and
metabolic eg aspirin overdose causing metabolic acidosis and respiratory alkalosis
ALCOHOLIC KETOACIDOSIS
In this case the patient had normal lactate levels and renal function with no other co-ingestants. The
UA showed initially small ketones – repeated with moderate ketones.
Ketones on dipstick was 6.4 (see below). The patient was given IV dextrose and later insulin IVI in
addition to analgesia
Alcoholic ketoacidosis (AKA) is an uncommon and frequently missed condition & as the signs &
symptoms a patient with alcohol abuse presents with may be fairly non specific (abdo pain,
vomiting, dehydration), the diagnosis may not be recognised.
In general patients with AKA present post binge when the patient stops drinking. After the binge,
appetite is often poor due to pain, fullness, vomiting etc. A starvation state develops with ketosis
developing from fatty acid breakdown, complicated by dehydration from poor oral intake and
vomiting. The patient presents with a high anion gap metabolic acidosis, vomiting, and signs of
chronic ethanol abuse.
AKA can develop in chronic alcoholics, but even in those who are relatively novice drinkers.
AKA results from a complex interaction of ethanol metabolism, decreased caloric intake, volume
depletion, and counter-regulatory hormones (eg, cortisol, glucagon).
3 mechanisms, which result in a relative deficiency of insulin with respect to glucagon, are thought to
produce the state:
1.
a lack of oral intake results in a depletion of glycogen stores. The body's starvation response
includes a release of counter-regulatory hormones (epinephrine, cortisol, growth hormone), a
decrease in serum insulin levels, and an increase in serum glucagon levels.
2.
volume depletion may induce these counter-regulatory hormones, increasing glucagon levels
while suppressing insulin.
3.
the oxidation of ethanol produces acetaldehyde, which is oxidized to acetate. Both steps in this
process convert nicotinamide adenine dinucleotide (NAD) to the reduced form of nicotinamide
adenine dinucleotide (NADH), increasing the NADH/NAD ratio. This reduces hepatic
gluconeogenesis, further reducing glucose levels. Hence, insulin levels remain suppressed, and
serum glucagon levels remain elevated.
The metabolism of alcohol itself is a probable contributor to the ketotic state.
Ketone production is a protective mechanism during starvation to provide energy to the brain and
other tissues.
After consumption of available glycogen the body switches largely to fatty acids as a source of
energy.
In contrast to fatty acids, ketones can pass the blood-brain barrier to deliver energy to this organ.
In early starvation ketones are also used for energy by muscle cells but later these convert to fatty
acids to conserve ketones for the brain.
These mechanisms assist in preserving carbohydrate supplies for cells dependent on sugars for
energy supply such as red cells and the renal medulla.
The ketones which may be found in the circulation are acetoacetate, beta-hydroxybutrate and
acetone. They are produced in the liver in an environment of low insulin and low intracellular
carbohydrate as an adaptive mechanism to provide non-carbohydrate fuel for the brain and other
tissues in times of starvation.
Acetoacetate is produced from acetyl CoA and may then either be converted enzymatically to betahydroxybutyrate or non-enzymatically to acetone. The interconversion of acetoacetate and betaEditor: Peter Wyllie
hydroxybutyrate requries the enzyme beta-hydroxybutyrate dehydrogenase and the ratio of the
two metabolites depends on the prevailing concentrations of NAD and NAHD.
The patient may complain of the following:
 Nausea, vomiting, hematemesis, and/or abdominal pain (each found in 60-75% of patients)
 Dyspnoea, tremulousness, dizziness, and/or hematemesis (10-20% each)
 Muscle pain, fever, diarrhoea, syncope, seizure, and/or melaena (1-8% each)
Examination usually reveals signs of alcohol abuse and dehydration. Shock related to volume
depletion may be present. The mental state may be impaired. There may be abdominal pain
related to pancreatitis.
Investigate with baselines FBC, EUC, BSL, LFTs, amylase / lipase, coagulation studies, blood culture
if infection is suspected; CXR (aspiration, infection or if tachypnoea is present). Ensure a bedside
Dextrostix and correct hypoglycaemia urgently.
Arterial blood gas examination may reveal a mixed picture
Blood gas- venous or arterial
ABG may show a low PCO2, low bicarbonate, and normal partial pressure of oxygen (PO2).
Serum pH may be misleading because the patient with AKA actually may have a mixed acid-base
disorder. In addition to metabolic acidosis due to ketone formation, a metabolic alkalosis may be
present due to vomiting and volume depletion. A respiratory alkalosis may be present secondary
to hyperventilation. The possibility of a double or triple acid-base disorder means serum pH may
be near normal despite a severe acid-base disturbance.
Urinalysis: UA for ketones may be negative or only weakly positive because the
nitroprusside test detects acetone and Acetoacetate but not beta hydroxybutyrate. In
AKA hydroxybutyrate production is favoured over acetylacetate in a ratio of 5:1. As treatment
progresses this ratio shifts and with improvement the UA test for ketones may become more
positive as increased amounts of acetylacetate are produced.
The anion gap is elevated.
Metabolic acidosis may also be due to lactic acidosis.
Hyponatremia and hypokalemia have been reported in patients with AKA.
Treatment
Begin with oxygen administration and ensure adequate ventilation (note altered LOC may be
present).
Begin volume resuscitation if the diagnosis is suspected.
All alcoholic patients require thiamine to prevent the development of Wernicke’s.
All patients with severe AKA are dehydrated. Several mechanisms are responsible for dehydration,
including protracted vomiting, decreased fluid intake, and inhibition of antidiuretic hormone secretion
by alcohol. Dehydration is a stimulus to the sympathetic nervous system and is responsible for
elevated cortisol and growth hormone levels. Dehydration and volume constriction both decrease the
ability of the kidneys to excrete ketoacids. Shock and lactic acidosis can develop.
Once shock has been corrected rehydration with 5% dextrose and N Saline should occur.
Carbohydrate and fluid replacement (in the form of 5% dextrose in normal saline) reverses the
pathophysiological derangements that lead to AKA.
Replenishing carbohydrates and fluids increases serum insulin levels and suppresses the release of
counter-regulatory hormones and glucagon.
Dextrose stimulates the oxidation of NADH and aids in normalizing the NADH/NAD ratio. Fluids
alone do not correct AKA as quickly as fluids and carbohydrates together.
Consider K, Mg replacement as resuscitation progresses.
Phosphate depletion is also commonly present in alcoholics. The plasma phosphate concentration
may be normal on admission; however, it typically falls to low levels with therapy as insulin drives
phosphate into the cells. When present, severe hypophosphatemia may be associated with marked
and possibly life-threatening complications, such as myocardial dysfunction, in these patients
Bicarbonate therapy should be considered only in the face of severe, life-threatening acidosis (ie, pH
<7.1) that is unresponsive to fluid therapy.
Evidence of pancreatitis is found in most patients, and many exhibit impaired glucose tolerance or
mild type II DM after recovery from the acute episode.
Editor: Peter Wyllie
Unless the patient has prior diabetes or other reasons as to whuy they not produce insulin in
response to the dextrose load, routine insulin administration is not recommended.
The initial management should be in a high dependency setting till there is documented improvement
in the metabolic state as indicated by an improving pH. In the patient with profound acid base
disturbance, ICU admission may be initially required.
Evaluate the patient for signs of alcohol withdrawal syndrome, which may include tremors, agitation,
diaphoresis, tachycardia, hypertension, tremors, agitation, seizures, or delirium. Exclude other causes
of autonomic hyperactivity and altered mental status. If the diagnosis of alcohol withdrawal syndrome
is established, consider the judicious use of benzodiazepines, which should be titrated to clinical
response. An alcohol withdrawal scale should continue to be monitored throughout the admission and
D&A services should be involved early.
Ketone Meter (Optium®)
Acetoacetate (AcAC) is either converted enzymatically to beta-hydroxybutyrate (BOHB) or nonenzymatically to to acetone. AcAc and BOHB are moderately strong organic acids;
acetone is an inert, volatile chemical. The BOHB/AcAc ratio is normally 1 to 2:1, and
may reach 6 to 10:1 in DKA .
Note, the urine analysis sticks use a nitroprusside reaction which detects Acetyl Acetate. Acetone is
approximately 1/20 as reactive as AcAc but nitroprusside does not react with beta hydroxybutyrate.
AS mentioned above in AKA hydroxybutyrate production is favoured over acetylacetate yet as
treatment progresses this ratio shifts and with improvement, the UA test for ketones may become
more positive as increased amounts of acetoacetate are produced.
The ketone meter however detects beta-hydroxybutyrate, and thus is more reliable in
detecting the relevant ketone bodies at a earlier stage as you don’t have to wait for the
patient to pass urine.
The meter takes ~ 30 seconds to provide a result.
Due to cost reasons the people who it should be performed on are all sick diabetics or alcoholics or
sick patients found to have hyperglycaemia (new Dx of diabetes).
The below values and recommendations from the manufacturer for insulin dependent diabetics
- <0.6mmol/L
- 0.6-1.5mmol/L
- 1.5-3.0
- > 3.0
- normal
- mild hyperketonuria – extra insulin ~15% with adequate carbohydrates
– “impending DKA” – extra insulin ~20% with adequate CHO
– seen with DKA
You need to look at each case individually but looking at these suggestions, I’d be checking a venous
pH with all pts > 1.5 till we get a feel for the significance of those values 1.5-3.0.
For those on insulin infusions for DKA or the AKA patients, I’d also be repeating the test every 4 -6
hrs looking for some improvement particularly after the acidosis (as reflected by the BE and
bicarb – knowing that patients have a respiratory compensation) has resolved.
Take Home Points:
 Calculate the anion gap when assessing metabolic acidosis – DULSI / USED CARP are the 2
mnemonics to remember
 Consider alcoholic ketoacidosis as a differential and use the ketone meter- UA is limited in
value

Treat AKA with good supportive management with a focus on extra carbohydrates, thiamine
and electrolyte correction (esp K and PO4) -
Editor: Peter Wyllie
JOKE / Quote OF THE WEEK
NEXT WEEK
A colleague at RNSH treated where they had a 50yo cyclist who came off his bike, smashed his
helmet and was amnesic and bruised and battered. The complicating issue was that he had a deep
brain stimulator in place to manage his Parkinson's disease tremor. What are the implications of this
to us in the ED ?
Please forward any funny and litigious quotes you may hear on the floor (happy to publish names if
you want)
THE WEEK AHEAD
Tuesdays - 11.30-2.30 Intern teaching -Thomas & Rachel Moore
Wednesday
0800-0900 Critical Care Journal Club. ICU Conf Room / 12.30-1.30 Resident MO in
Thomas & Rachel Moore
Thursday 0730-0800 Trauma Audit. Education Centre / 0800-0830 MET Review Education centre /
1300-1400 Medical Grand Rounds. Auditorium.
Editor: Peter Wyllie