Archive for the ‘Case Studies’ Category

ventricular tachycardia and methadone

Sunday, June 20th, 2010

A 42 year old male with a past history of IVDU and alcohol abuse and brain injury, presents with what looks like withdrawal. Current medications included methadone and earlier on the same day, he was commenced on naltraxone.

Initially he is found to be becoming progressively more agitated and having brief episodes of depressed conscious state, with improvement between. He is ‘jittery’ with myoclonic movements in the bed. On vitals, he is found to be afebrile with a fluctuating Glascow Coma Score, bradycardic, and to have a systolic blood pressure of 80mmHg, and so he is taken to a resuscitation cubicle.

Is he in withdrawal?
Is he seizing?

As I enter the resus cubicle to find out why the patient is there, I notice a wide complex tachycardia at a rate of about 230bpm. He is still moving. It is self limited after a few seconds. Then a further episode.

In between episodes we do this ECG:
img_05523

It shows a bradycardia at rate 42bpm, there are tall T waves and premature ventricular complexes. There is a hint of a sinusoidal wave form in V2-V3(but no bundle branch, so not Brugada).
Is it ischaemia?
The QTcorrected. It’s 524ms. A QT corrected of greater than 450ms is considered prolonged.

The diagnosis is; prolonged QT causing Torsades.

Here is the next ECG we take as he begins an episode.
img_0553

So now we see a bizarre wide complex tachycardia, that looks like Torsades, with very abnormal QRS complexes following and the telltale signs of of patient shaking and agitation.
It is self limiting.

We commence Magnesium infusion in this patient. His K is 3.5, so we increase that also.

He then has a further episode which is on the rhythm strip below:
img_0555

He needs cardioversion for this.
He is intubated and soon stabilises. We do one more thing and that is, get a head CT. Why do we do this? There are a small number of cases where increased intracranial pressure can cause prolonged QT. Given his history of IVDU and alcohol, we want to exclude a subdural, or other lesion.

It is normal.

Cardiology review prior to stabilisation and want isoprenaline to increase the heart rate.
Why do they want this? ………..Read on.

Let’s look at QT prolongation.

It is caused by:
-hypomagnesemia
-hypokalaemia
-hypocalcaemia
-Na channel blocking drugs, such as Type I drugs
-raised intracranial pressure
-acute coronary syndrome
-hypothermia
-hereditary causes such as Lange-Nielsen(QT and deafness) and Romano-Ward(no deafness)

Management is Magnesium and in more severe cases of recurrent Torsades an implated defibrilator.

WHAT CAUSED THE QT PROLONGATION IN THIS PATIENT?

Most probably Methadone.
It is a synthetic opioid that is metabolised by the cytochrome P450 pathway and affects Potassium ion channels.
Studies have found that it causes significant increases in the QT interval (Martell et al, Am J Cardiol 2005;95:915-918)(Krantz et al, Pharmacotherapy 2005;25:1523-1529), especially in those on a maintenance dose greater than 40mg/day.

Why was isoprenaline recommended by cardiology? Quite clever really…
We know that Torsades is caused by QT prolongation, so increasing the heart rate decreases the QT as per the following formula:
QT = 656/[1+(heart rate/100)] (Ravtaharjus’s formula)

The patient stabilised on Magnesium and Potassium, without isoprenaline and he went to an ICU bed, with a plan to manage and substitute his Methadone.

So beware the IVDU patient on methadone that presents with syncope. We often put the symptom down to the patient having used heroin or a similar drug. Do an ECG and look for a prolonged QT, although uncommon, it may have been an episode of Torsades de Pointes.

Peter Kas

Posted in Cardiology, Case Studies, Resuscitation | Comments Off

How good are we at predicting ischaemic chest pain?

Monday, May 24th, 2010

lbbb-with-inferior-stemi-cropped

Here’s a case I had recently:

62 year old male presents to the Emergency Department with what he calls a flare-up of his congestive cardiac failure. He states he is short of breath. He is a frequent presenter to the department with this complaint. He has not taken his frusemide for the past 48hours.

He states that he feels very tired.

His examination is as follows:

He is a well looking man with normal vitals

Heart sounds dual, no murmur. normal JVP, bilateral pitting oedema to mid calves.

Chest clear

Abdomen soft

His ECG and CXR are normal

Bloods including a troponin are normal.

I’m unsure of the diagnosis, but given he hasn’t taken his frusemide, I treat him with that.

I am going to discharge him, however it is late at night and he lives alone, so we decide to keep him in the department overnight.

In the morning, he looks well and feels better, but still lethargic, ECG is unchanged, but for some reason someone does a follow-up troponin and it is 4.

He is diagnosed with a NSTEMI and sent to cardiology.

So the question I posed was, “How good are we at diagnosing cardiac chest pain?” and “Are there some signs or symptoms such as shortness of breath that are more important than we may initially think they are?”

Pope et al(NEJM 2000;343:1167-1170) looked at the rate of missed diagnoses of cardiac ischaemia in the emergency department.

This was a study of some 10689 patients and the conclusion was that there was a subgroup of patients more likely not to be admitted, who had ischaemia or infarction.

Those more likely to not be admitted were:

-Non-whites

-Females less than or equal to 55 years of age

-Those with shortness of breath as their only complaint

-Those patients with a normal ECG.

Chadwick et al (Ann of Emerg Med 2004;44:565-574) looked at the question of our initial diagnostic impression as clinicians and if it was adequate in excluding cardiac disease. This was a prospective registry-based study, conducted at eight hospitals. They evaluated patients where the physician’s impression was that the cause of chest pain was not cardiac. Patients had a 30 day follow-up and adverse events included STEMI, NSTEMI, going to the cath lab or death were collated.

Of the nearly 3000 patients in this study, a minimum of 2.8% a potential maximum of 6.3% of those being clinically ruled out of having ischaemic chest pain, had a cardiac event. What was interesting was that 53.2% of patients who had been labelled as non-cardiac, still had a cardiac marker workup.

Factors that were found in this study, to be significant in predicting those patients with a cardiac event were:

-Past history of coronary artery disease

-Age

-Diabetes

-Hypercholesterolaemia

-History of Congestive cardiac failure

-Feeling of ‘weakness’ correlated highly.

So beware the patient who presents with shortness of breath or weakness as complaints. Lethargy or fatigue, is especially common in the elderly, and this is the group to be most aware of the diagnosis in.

The above list is similar to the American Heart Association list, that lists the following as being important factors in the initial diagnosis:

-The nature of the presenting angina- This is critical. If a patient gives me a great story of angina, I don’t care if they have risk factors or not, they need to be assessed by cardiology as the story means everything.

-Past History of coronary artery disease

-Male

-Age

-Number of risk factors

There are also presentations that result in a lower likelihood of ischaemia and they include:

-reproducibe pain on palpation

-Positional pain

-Pleuritic pain

-Stabbing pain

-Pain radiating to the lower limbs

How good is the ECG at helping us?

We know that up to 50% of cases with acute myocardial infarction(AMI) have a normal ECG at presentation. Serials are important. What is more important is that the ECG is probably more significant than all history and examination put together and a normal ECG predicts a group of patients with a lower rate of complications.

Thomas et al (NEJM;2000:342;1187-1195) evaluated patients with acute chest pain. AMI was present in 80% of patients with ST elevation of greater than, or equal to 1 mm and in 20% of patients with ST depression or T wave inversion. With a totally normal ECG, the risk of AMI was 4%, if there was a history of coronary artery disease and the patient had chest pain and 2% if no past history.

How about other subtle presentations?

My patients will often describe the chest pain as indigestion, or they tell me that the chest pain makes them want to belch. Are these patients fine to discharge? Here are a few facts:

-About 20% of patients with an AMI describe their pain as that of ‘indigestion‘

-About 50% of patients having an AMI had belching associated with pain.

But surely, if I give them a GI cocktail(mylanta and xylocaine viscous) and the pain goes away, that should be enough? As it turns out , the GI cocktail has been found to have the same effect on ischaemia as it does on reflux(Ann of Emerg Med 1995).

So what does all this mean? Are we now going to admit everyone? No. We are still going to risk stratify. We know that despite our best efforts that we will all miss up to about 2% of cases. The purpose of this blog is to look at all those patients with more subtle presentations.

So in Summary:

-Beware the patient with shortness of breath as their only complain, especially if elderly or a diabetic, as it could be ischaemia.

-Beware the patient presenting with lethargy or weakness, especially if they are elderly, they may have ischaemia.

-Beware the diagnosis of reflux, as symptoms of belching or pain even described as that of indigestion, can be cardiac.

-Pay attention to the story. If that is a good one for angina, nothing else matters.

Next time we’ll look at the same case from the viewpoint of it potentially being a pulmonary embolism.

-

Posted in Cardiology, Case Studies | 1 Comment »

PROPRANOLOL OVERDOSE

Thursday, July 9th, 2009

This  case study on beta blocker overdose was presented by one of our registrars, at Grand Rounds. It was an interesting case and one we thought you might enjoy.

A 53 year old male is brought to the Emergency Department by ambulance:

At 2045 he had taken an overdose of his beta blocker medication.

The ambulance was called at 2101 and arrived at 2121

The patient was found to be alert with a pulse rate of 54 and a blood pressure of 80/66.

He was cannulated and transferred

En route, his GCS decreased to 11/15 and he was hypotensive and borderline bradycardic. On arriving in the ED he had a tonic clonic seizure.

It was ascertained that he had taken 100 of his 40mg tablets of propranolol ie., 4g of propranolol.

The seizure terminated and then the patient was found to be in PEA ie had a rhythm but no output.

He was intubated and treated as per ALS with Atropine and Adrenaline.

Return of Spontaneous circulation occurred after 3mg of adrenaline.

The issues were his bradycardia and moreso persistent hypotension.

He was treated with:

-4mg of glucagons IV x 3 doses- which later became an infusion

-Isoprenaline infusion- quad strength

-Intermittent adrenaline boluses

-Insulin dextrose boluses

He then further had:

Adrenaline infusion

-Noradrenaline infusion

Actrapid at 50U/hr

All to maintain a heart rate at 57 and a BP at 96/45

I hope you are beginning to see that Propranolol OD can be incredibly difficult to manage.

But that’s not all:

He was then transferred to cath lab for a pacing wire and transferred to ICU where his Actrapid infusion was tripled to 150U/hr.

In ICU he was gradually weaned off the infusions. He continued to have intermittent seizures which were treated with clonazepam

His course was also complicated by a left lower lobe pneumonia.

His was discharged from the hospital 16 days after the OD

Lets look at Propranolol overdose.

Propranolol is a non-selective beta antagonist. It has high membrane stabilizing capacity and is lipophilic.

How do we manage these patients?

For Fellowship candidates here’s the mantra: Resus cubicle with non invasive monitoring including cardiac monitoring, non-invasive blood pressure and oxygen.

We go through the same ABC approach always.

AIRWAY and BREATHING

Make sure the airway is secure. In many cases the lipid soluble nature of propranolol results in seizures and a decreased conscious state.

In these cases seizure management will occur first(or sometimes in unison) with securing the airway.

IV access early is important in these patients. Seizure control will usually be established with benzodiazepines PRN. Phenytoin in many cases is ineffective in controlling further seizures.

With IV access and airway and seizure control, circulation control and support becomes paramount. First lines of treatment are fluids, fluids, fluids and atropine, understanding that atropine may not be effective.

Gastric decontamination may not be very useful in these cases and although charcoal may not very effective, it is certainly something to try if the airway is secure.

What INVESTIGATIONS do we perform?

LABS

Basic bloods won’t add much to the picture

Blood gas and lactate may be important as worsening acidosis increases the predisposition to arrhythmias

BSL-hypoglycaemia is rare, hyperglycaemia has been reported.

How about as ECG?

Well its good if we look at QRS duration.

BEDSIDE ECHO?

Certainly in the haemodynamically challenged patient it can add some information.

If the heart is hypodynamic, inotropes may be needed, if normodynamic, pressors may assist.

Our aim in management is circulatory support and organ perfusion. So some of the parameters we may be looking for are:

-EF>50%

-SBP>90mmHg

-Euglycaemia

-Normal pH

-QRS <120ms

-Good Urine output(so make sure you get an IDC in the intubated patient)

SO WHAT ARE THE TREATMENT REGIMES?

Catecholamines

-all have been used in beta blocker OD with varying degrees of success. One important characteristic is that massive doses(quad strength) are needed for any clinical effect. Several case reports have shown in some cases of high dose or multiple catecholamines in restoring perfusion.

Calcium

-There is a suggestion in animal models that Ca improves inotropy and blood pressure but not conduction or rate.

Kern(Emerg Med Clin N Am 2007) suggests a Calcium bolus of 0.2ml/kg of 10% Ca Gluconate and then an infusion of 0.2-0.5ml/kg/hr titrated to effect-the aim being twice the normal serum calcium. Beware here as there is a potential for harm.

Glucagon

-It stimulates intracellular adenyl cyclase via non adrenergic receptors and has been described for the treatment of of beta blocker overdose, with the intent of inotropy as far back as 1973.

-It is usually given in up to 5mg boluses prn and an infusion then started , as a rule of thumb, at the effective bolus dose per hour.

-The one problem with this is that we run out of it very quickly in terms of hospital supply.

Insulin and Euglycaemia

-A far back as 1986 insulin was recognized as exerting significant inotropy(Reikeras J Card Pharm 1986) This was through a shift in cardiac metabolism from free fatty acids to carbohydrates and an increased glucose uptake. There have been animal model studies showing superiority of insulin to adrenaline/vasopressin.

-The proposed dosage is an initial bolus of 1unit/kg with 50ml 50% dextrose and then an infusion of insulin and dextrose at a rate of 0.5 U/hr titrated to euglycaemia.

-Beware it may not work right away and could up to 15 minutes to work, so start early.

IS THAT ALL?

I’m sure that there’s a lot more that can be done, and the toxicologists out there are ready to add their bit. This certainly can be done on the ‘blog’ on resus.com.au where this case study has been added.

What about unmanageable hypotension? Think about extracorporeal elimination.

Posted in Case Studies, Toxicology | 1 Comment »

The Septic Baby

Tuesday, June 16th, 2009

Case Study: Paediatrics
—————————————————————–
A 5 month old male baby was brought into the Emergency Department by his mother.

He is lethargic and limp with occasional aggravated-type crying. The conscious state is alternating between being asleep and agitated crying. He was not quite himself yesterday according to the family.  Today he went off food three hours ago, quite rapidly and since then has been as we see him now.

There is no past history, normal vaginal delivery and immunizations up to date.

Vitals are:

1. PR 234 bpm
2. Temperature 38°
3. BP - trouble getting
4. RR 40/min

What do people think?

The important thing to say at outset is that this is a sick baby. The more rapid and sudden the outset of illness, the
potentially sicker the baby is.
So some comments about the vitals:

1. PR 234 bpm (really tachycardic- for anyone)
2. T 38° febrile
3. RR within range

So what are some normal figures? I’ve shared the way I calculate weight before. The way I remember is this.

1. 1yr - 10kg
2. 3yr - 15kg
3. 5yr - 20kg
4. 7yr - 25kg
5. 9yr - 30kg
What about smaller children?

1. Birth - 3.5kg
2. 6month - 8kg

If you remembered 3.5, 7, 10, 15, 20, 25, 30, you would be okay.

What about pulse rate?

Well 234bpm is high for anyone.

I remember that children from

Birth to 1 year 170bpm

0-1yr 170bpm

1        170bpm

3yrs 150bpm

5yrs 130bpm
7yrs 110bpm
9yrs 110bpm    Can you see the pattern?- reducing by 20 every time until 9

Now there are ways you can get all these values. They may be on your computer, or a ‘tape’ or somewhere you personally keep this data, like an organiser. The reason I teach the simple ways to remember things is that you may not always be at the hospital you know, you may be in another hospital, where you can’t get rapid access to this material.

Respiratory rate is within normal limits.

We were not able to get a BP - this at the time was probably a mechanical issue.

What other readings are important here?

1. Take a BSL (it was 5.1)

2. The other thing to do is capillary refill.

The other thing we need to beware of is that the tachycardia is not SVT.  The ECG demonstrated a regular marrow complex tachycardia with P waves - so this was a sinus tachycardia.

So how did we approach this child?

The baby was already in a resus cubicle with monitoring attached.

We checked:

Airway - the baby was crying which indicated an intact airway- There was no stridor or other sound.

Breathing - There was good air entry, no tachypnoea and the sats were 98% on room air

Circulation - This is the critical part here. The baby was tachycardic which was a response attempting to maintain cardiac
output. Remember and beware of bradycardia as this may also occur and is a potentially critical sign such that it may precede
asystole.

BP is good to take, however hypotension is a late sign and the child may be normotensive and in trouble.

Capillary refill is a useful sign - press for about 5 seconds and let go. Can use the finger, or can use the area around the
wrist.

* Refill < 2 sec = normal
* Refill 2-4 sec = delayed and means a fluid deficit.

Disability
Next we need to assess the child in terms of neurological states, and we can use the AVPU formula.

* Awake
* Verbal response
* Pain response
* Unresponsive

This baby was awake.

Exposure

This baby had a minor blanching rash on the right foot and nil else.

ENT examination was normal.
As we look at the ABC I remember also being taught DEFG: “Don’t Ever Forget Glucose”.

If the glucose is low we give 5ml/kg of 10% dextrose.

So how did we manage this baby?

We recognised early that this was a sick septic baby with potential shock.
It is important in septic shock to treat the infection as a matter of urgency.

* We had established airway and breathing were okay.
* We established IV access - We got this on first attempt. If we didn’t get it on first attempt we would try one more time then
intraosseous would be attempted.
A word on intraosseous:

* What types are there? - There is the cannula type with stylette and there is the drill-type
* Where do we insert? - medial to proximal tibia about 1cm below tibial tuberosity to miss the epiphysis (can use distal femur)
When you aspirate you get marrow. Remember that in children older than 5yo the marrow becomes fatty and aspiration may not be possible.

There are the expected potential complications

* trauma (may penetrate posterior cortex, multiple attempts can result in extravasation)
* infective - cellulitis, osteomyelitis
* can also get compartment syndrome

Take bloods when IV in: need FBC, EUC, Venous gases, lactate, Blood Cultures

Give fluid as bolus
- if child is obtunded, 20ml/kg N saline

We give 2x 10ml/kg bolus (why? I don’t know)to this child as he was not totally obtunded.

While this was being done we took a urine specimen by catheter.

This was positive for leukocytes ( it lit up).

We gave antibiotics - cefotaxine 50mg/kg and we added gentamicin 7mg/kg. With the antibiotics etc, the baby had a total input of about 30ml/kg of fluid.

We consulted with paediatrics early and the paediatric consultant also agreed with our management.

At all times we kept mum, dad and grandma there and informed. At every step we spoke to them about what we were doing and what to expect. We also explained why we were doing what we were; why the antibiotics were being given etc(Take note Fellowship candidates)

Over the next 30mins:

- the heart rate decreased
- the baby settled and was more alert. Soon after this he was interacting, smiling and playing.

This was a very quick recovery, but you sometimes see that.
Bloods showed mild acid base imbalance and increased WCC

The point is - get antibiotics and fluids in quickly in a flat baby.

Somebody asked the question - would you lumbar puncture?

My answer was NO for two reasons:

1. we found infection in urine
2. LP may not be the best investigation if there is any question of altered level of consciousness, prior to excluding space occupying lesion.

Posted in Case Studies, Paediatrics | 2 Comments »

Vertigo part 2- video of Head Thrust Test

Tuesday, June 2nd, 2009

I recently spoke about the head thrust test, to differentiate peripheral from central causes of vertigo.

Here is a video demonstrating it.

Remember that the vestibulo-occular reflex is affected on the side opposite to the quick phase of the nystagmus.

Posted in Case Studies, Neurology/Neurosurgery | No Comments »

The Glue Sniffer’s Mother- A case study

Wednesday, April 29th, 2009

Some people have asked me to present an old case I put up at the “Airway, CPR and Trauma” workshop. This is a case I saw as a registrar, simple and effective for teaching.

A 56 year old woman presents after midnight to the ED. She says that she is having an anxiety attack, brought on by the fact that her son is sniffing glue.

The patient is triaged as a Cat 4.

When seen she is sitting up in bed, alert, stressed, but not distressed. She is tachypnoeic with dry lips.

She gives a past history of anxiety attacks similar to this, but no other past history. She states she is not on any medications and has no allergies.

On examination, her vitals are:

  • T 35.9 degrees celsius
  • BP 160/85
  • HR 110
  • RR 40
  • Sats 99% RA

She is alert. She has dual heart sounds and her chest is clear with equal air entry. Her abdomen is lax and she has a normal rapid neurological examination.

So in summary someone who has come in claiming an anxiety attack for a known reason, and an attack similar to previous one, with some tachypnoea and tachycardia.

The impression is an anxiety attack and the approach taken with this patient was reassurance, a discussion of her son’s drug taking habits, a small dose of diazepam, with review planned and possible psychiatric review.

Reasonable? Would anyone do anything different?

Obviously there’s more to this case given that I’m presenting it here.

When the patient is reviewed, approximately one hour later, she is still tachycardic with a pulse rate of 110bpm. She is still tachypnoeic.

The only difference is that she is now complaining of Pleuritic Chest Pain!

Alrighty then! What do you do now?

Well, I move her to a resus cubicle, apply non-invasive monitoring, high flow oxygen, put in an IV and take bloods (for all Fellowship candidates, this is the mantra) and…what other investigations?

What are your differentials?

Remember tachycardia, tachypnoiea and pleuritic chest pain. Well it should include:

  • pulmonary embolism right up there.

What else?

  • pneumothorax
  • chest infection
  • pleurisy

What else?

So what do you want to do next?

I hear someone say CXR.

Well, there was an incidental finding of a right upper lobe nodule, but that’s it.

ECG was also normal except for tachycardia.

What other investigation would you do?

Well I’ll tell you what I did - ABG’s ( on 6LO₂).

This was the result:

pH - 6.886 (7.35-7.45)
pCO₂- 8.2 (35-45)
pO₂- 139.5 (75-100)
HCO₃- 3.8 (22-26)
Sats - 94.2% (94-100)

Okay all you Fellowship Candidates, interpret this:

Whilst you’re thinking, the way I always look at this is to understand it first. This lady is acidotic, with a low pCO₂, because she is breathing so fast. Her HCO₃is low, more than likely because she is using bicarb because she is so acidotic.

So if we again look at her pCO₂, if this was higher she would be even more acidotic, so her tachypnoea is probably a compensatory measure.

So the gases are: “Partly compensated metabolic acidosis with corrected hypoxaemia”.

So what causes are you starting to think about?

To help us further, the other blood tests have now returned.

Full Blood Count: Normal
Electrolytes: Na 132
                       K 5.4
                       Cl 106
                       HCO₃4
                       Cr 13
                       Ur 11.4

What one other bedside test would you now do? Let’s first calculate the ANION GAP.

Remember, plasma should have no change. Na change must be balanced. If HCO₃and Cl cannot do that, there must be unmeasured anions…there are also unmeasured cations.

Anion GAP = 132- (106+4) = 22 HIGH

So this patient has a WIDE ANION GAP METABOLIC ACIDOSIS. What was the other bedside test to do?

I did a BSL. The sugar was 33.2 mmol/L.

Diagnosis?

Yes Diabetic Ketoacidosis.

Urine = Ketones.

Remember the four causes of Anion Gap Metabolic Acidosis are:

-Renal failure,

-Ketoacidosis,

-Lactic acidosis and

-Exogenous poisoning.

The patient’s partner arrived soon after this and gave a more accurate history.

The patient was in fact a NIDDM, on insulin for 2 years, but not taking her insulin. On top of this, she has been eating large quantities of ice cream!

Other past history includes:

  1. HT
  2. Hypercholesterolaemia
  3. DKA
  4. Bilateral Pulmonary Emboli following DKA (had been on Warfarin but this was ceased 3 weeks prior due to poor compliance)

JACKPOT!

The rest of the story was that she was currently supposed to be taking ‘Mixtard’, ‘Ramipril’ and Simvastatin.

Her social history was that the patient and her de facto were invalid pensioners, who live in government housing.

One more thing…the patient’s son actually DOES SNIFF GLUE!

MANAGEMENT

My management of this patient, in brief was:

  • IV fluids
  • Actrapid infusion, initially at 7 U/hr
  • Potassium supplementation
  • Bicarb - although controversial, it was given as per hospital endocrine protocol

The patient was admitted to a HDU bed.

A FEW WORDS ON DKA

Although no exact definition exists, certain criteria are suggested and include: pH < 7.3, Glc > 13.8 mmol/L, HCO₃< 15mmol/L, High Anion gap, positive serum ketones.

It is rare to have an insulin dependent type II diabetic with ketones and DKA. The mortality of DKA is less than 5% compared with 30% in Non-Ketotic Hyperosmolar Syndrome.

The Aetiology?

  • Non-compliance
  • Infection
  • Stroke
  • MI
  • PE
  • Trauma

Note that no cause is found in 25% of cases.

TREATMENT

Fluid

Patients can be severely dehydrated, sometimes 5L+.

If there is no hypotension, give 250ml/hr of normal saline.

If hypotension is present, resuscitate accordingly knowing that the deficit can be up to 100ml/kg.

Insulin

Give a bolus of 0.1 U/kg IV then place the patient on an infusion of 0.1 U/kg/hr. Continue this until ketonaemia resolves, or the anion gap normalises.

Remember that in a small group, some 1-2% the insulin infusion rate may have to be increased as they are ‘non-responders’.

Potassium

Beware as patients with DKA have a total body potassium deficit. Ensure there is urine output and be alert to dropping levels as the insulin drives it back into the cells.

I start replacement with 10mmol/hr when the potassium falls below 5.

Magnesium

Beware its depletion through diuresis, although not an acute problem.

Clinically look for hyper-reflexia, or a Chvostek or Trousseau sign.

Bicarbonate

This is still controversial as no study has really demonstrated improved clinical outcome. The result of supplementation may include worsening hyperkalaemia, intracellular acidosis and precipitation of cerebral oedema.

It will usually be found that the more severe the acidosis, i.e. ph <7, the greater the need for gentle replacement.

——-

There it is, a brief look at DKA and an interesting case study!

 

 

 

 

Posted in Case Studies, Endocrine | No Comments »

Vertigo and Nystagmus

Friday, April 3rd, 2009

Nystagmus

A 65 year old man presents to the emergency department with a sudden onset of ‘dizziness’. He feels more dizzy on any head movement as well as on sitting up. He is finding it difficult to walk around as his balance is affected.

This is a common presentation in emergency departments and our main role here is the determination of whether this is a peripheral or central cause. We know that in some cases central causes can be difficult to differentiate from peripheral. In this month’s ‘Medical Talk’ we go into “Vertigo and Nystagmus’ and discuss the means of determining the difference. We look at methods that have been in place for some time and then consider new advances.

A very common complaint of patients such as this one, presenting to the emergency department, is ‘dizziness’. In most cases the patient is referring to vertigo but we must clarify this. Vertigo is the perception of movement where there is none. The patient may move in respect to their surroundings or vice versa. The important thing to distinguish is whether or not this is a central or peripheral cause; this is where the challenge lies.

Vertigo is caused by a non-integration or non-correlation of inputs from our senses responsible for our spatial positioning. The sensory organs involved are:

1 vision- which determines our spatial orientation

2 proprioception - which determines body position

3 vestibular system - which determines our position in relation to gravity.

Inputs from these areas determine outputs that drive the vestibulo-occular reflex (VOR)

Nystagmus which is a clinical finding in most cases is of significant assistance in respect to making the diagnosis. Nystagmus is a rhythmical  movement of the eyes and has a fast and slow component. The side of the nystagmus is named after the fast component of the movement. The slow component is the result of the VOR. When speaking of determining a central or peripheral cause we are referring to horizontal nystagmus. Vertical nystagmus is always to be considered serious and in most cases is of brainstem aetiology.

Lets speak a little about the VOR. If you turn the head to the right quickly, the VOR is responsible for moving your eyes back to the centre. This has benefits in terms of maintaining focus on objects. The old discussion of ‘doll’s eye’ movement in brainstem death is related to patients that have lost the ability to move eyes back to centre. They are the dolls of old days where the eyes were painted on, so when the head is moved the eyes move with it- this is brainstem aetiology. So when the neurosurgeons come to your emergency department and turn the patient’s head from side to side and look at what the eyes are doing, this is what they are looking for.

This month in ‘Medical Talk’ we demonstrate a very helpful sign, the ‘head thrust’ test, which evokes the VOR. We look at dividing the causes of vertigo into a more clinical orientated rather than the time-old listing of potential causes. To all the guys that subscribe, enjoy the issue. It is posted out on Monday the 6th. We also cover our favourite(sarcasm) topic; atrial fibrillation in detail, detail, detail. Enjoy. For those that don’t get ‘Medical talk’ , join the club at $178 AUD for a year’s membership, it is probably the most value for money, emergency medicine investment, you will ever make.

Posted in Case Studies, Neurology/Neurosurgery | No Comments »

Why does this patient have numb feet?

Monday, March 2nd, 2009

This patient had Guillain Barre Syndrome. Listen to the patient give her history and then a short lecture on it.

Get the Flash Player to see the wordTube Media Player.

Guillain Barre Syndrome is an acute demyelinating polyneuropathy. Most cases follow some pre-existing infection up to three weeks prior. Causes may also relate to post surgery.

The patient will describe ‘numb’ hands or feet, as this patient in the audio above. The characteristic part of the condition is that it will progressively ascend.

The examination will demonstrate sensory loss and there will be a loss of reflexes within several days, although this will be present initially.

These patients will be investigated with lumbar puncture, which will be normal except for an elevated protein(although this may be normal initially).

Respiratory function tests must also be carried out to rule out respiratory failure.

Management is generally supportive with treatment with immunoglobulin.

Most patients will have a complete recovery. There is a small mortality rate, and the prognosis is not based on the level of protein in the CSF, but more on the progress of the disease ie., those bed bound early will have a worse outcome.

Posted in Case Studies | 2 Comments »

A case of Head injury that raised a few questions

Sunday, March 1st, 2009

CASE STUDY: TRAUMATIC BRAIN INJURY

A 30 year old male is brought to the Emergency Department with a traumatic brain injury. The history is an alleged assault with respiratory arrest following. He has been intubated by the paramedics and has been given adrenaline for hypotension. His pulse rate is 140bpm and his blood pressure is 95mmHg systolic.

Head CT

 

On arrival and after initial assessment there are several requests made by various members of the trauma team.

 

“Can we please give Mannitol”

“Should he have a vasopressor as his BP is low?”

“Can we please paralyse him?”

 

Which of these requests are valid and why?

 

Should we use mannitol?

The whole reason for using mannitol is to decrease viscosity and thus increase cerebral blood flow through osmotic diuresis. Does this increase cerebral perfusion pressure?

 Mannitol will work only with an intact blood-brain barrier. In fact current guidelines will only recommend its use in normotensive, euvolaemic patients with clinical signs of raised intracranial pressure.

 There is no evidence that dehydration in neurotrauma improves outcome. (Neurol Res 1999) To the contrary, the use of mannitol in hypotensive patients can affect cerebral perfusion pressures and lead to decreased perfusion which is an independent predictor of worse outcome. (J Trauma 1993).

 If indicated the doses warranted are 0.5-1g/kg.

 Certainly in this patient mannitol was not indicated as part of the initial resuscitation.

 A LITTLE BIT OF TRIVIA ABOUT MANNITOL

As recently reported in the BMJ, there is doubt directed at the original studies, three in total that support high dose mannitol. The studies were published in Neuroscience and Journal of Neuroscience between 2001 and 2004 and recommended 1.4g/kg on average of mannitol. According to Roberts who writes this article, the studies allegedly were conducted by Dr Julio Cruz  a neurosurgeon at the Federal University of Sio Paulo. Apparently the University denies ever having employed him, and his co-authors are not able to verify the patients used. Dr Cruz himself cannot be called on to support his studies as he apparently committed suicide in 2005.

 

 

USE Of VASOPRESSORS IN ACUTE BRAIN INJURY

There has been significant discussion about the use of vasopressors to increase Cerebral Perfusion Pressure(CPP)

CPP=Mean arterial pressure(MAP) – Intracranial pressure(ICP)

CPP has been proposed as being beneficial if  > 70mmHg

There is significant effect on autoregulation in head injury.

At present there is no significant evidence for the use of vasopressors in acute head injury. In fact the data indicates a worst outcome in this patient group.(J Neurosug 1995)

 

Should patients be paralysed?

There is evidence that long term paralysis use in patients may have a detrimental effect and should be used for those patients with known raised intracranial pressure.)Crit Care Med 1995)  In these patients with initial presentation and GCS of 3, following intubation, sedation may be adequate.

 

The CT showed extensive subarachnoid blood and a tight brain.

ICP was measured at 100mmHgHead CT

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