March 15, 2010

Cardiovascular Curveball #006

Consider a 49 year- old female with a history of smoking and two weeks of increasing shortness of breath. She is being treated for pneumonia on the ward for three days but getting worse. An ICU review is performed on the ward and the following ECG is obtained.

image 1 Cardiovascular Curveball #006

Click to enlarge

Q1. Describe the ECG findings. What investigation is indicated?

The most significant finding on this ECG is the presence of electrical alternans. The rhythm is sinus tachycardia at 100bpm and the axis is normal. The investigation indicated is an echocardiogram to confirm the presence of a pericardial effusion and to exclude pericardial tamponade.

Q2. You ring the cardiologist to arrange the investigation in question urgently and he asks you to assess the degree of pulsus paradoxus. What is pulsus paradoxus and what are the potential causes of this phenomenon?

Pulsus paradoxus is defined as an inspiratory drop of 10mmHg or more during normal breathing. It is caused by:

1. pericardial tamponade
2. hypovolaemia
3. acute asthma
4. massive pulmonary embolism

On the cardiologist’s advice you assess the degree of pulsus paradoxus and no significant respiratory variation in systolic pressure is present.

Q3. You run into difficulty getting the investigation you have requested in a timely fashion because the cardiologist argues that the absence of pulsus paradoxus is reassuring. Is he right?

In this particular case, no.

Electrical alternans is usually associated with tamponade and there are many reasons why pulsus paradoxus may be absent in the presence of cardiac tamponade including:

1. pericardial adhesions (particularly over the right heart)
— impede volume changes

2. severe left ventricular failure or marked left ventricular hypertrophy
— in these circumstances the pericardial pressure effectively equilibrates only with the right heart pressures with the much less compliant left ventricle resisting phasically changing pericardial pressure

3. right ventricular hypertrophy without pulmonary hypertension
— causes right-sided resistance to the effects of breathing

4. atrial septal defects
— increased venous return balanced by shunting to the left atrium

5. severe aortic regurgitation
— produces sufficient regurgitant flow to damp down respiratory fluctuations

References and Links

Metabolic Muddle #005

A 20 year old male presents with 3 days of lethargy and generalised malaise.  He is confused and looks very unwell.  The following blood tests are obtained:

image 11b Metabolic Muddle #005

Click on image to enlarge

Questions

Q1. Describe the acid base disturbance.

There is a severe metabolic acidosis with a raised anion gap with an appropriate degree of respiratory compensation.

Q2. What is the likely diagnosis?

Diabetic ketoacidosis

Q3. Describe the electrolyte abnormalities.

The patient has hypernatraemia and, in fact, is even more hypernatraemic than is immediately apparent. The glucose is very high and, therefore, a correction is required.

The calculation is:

[Na+] + (glucose -10)/3

In other words, the corrected sodium is 166.

The potassium is very low.  This is particularly noteworthy given the degree of acidaemia.  Acidaemia drives the potassium up so, as the acid base disturbance is corrected, the potassium will drop even further.  While total potassium deficits can be difficult to predict on the basis of serum potassium, the  total loss here is likely to be in the order of 100s mmols.

The magnesium is not low which would be unheard of in this setting unless the patient had received magnesium supplementation (which they had).

The phosphate is low – this too is a common electrolyte disturbance in DKA.  There is debate about the significance of low phosphate in this setting but Intensivists (myself included) can’t resist correcting the phosphate.

Q4.Should the corrected sodium be used for calculating the anion gap?

No. The anion gap reflects the balance between positively and negatively charged electrolytes in the extracellular fluid. Glucose is electrically neutral and does not directly alter the anion gap. However, glucose is osmotically active so water is pulled into the extracellular fluid. This has a dilutional effect on all extracellular electrolyte concenations, both positive or negative, and so the anion gap is minimally altered.

Q5. It emerges that the patient has recently been diagnosis with Schizophrenia and has commenced olanzepine. What is the significance of this additional history?

There are some data that suggest an increased risk of diabetes and diabetic ketoacidosis in patients commenced on atypical antipsychotics.

Q5. An amylase is measured and is found to be 3 times the upper limit of normal. What is the significance of this finding?

Mild elevations in amylase are common in diabetic ketoacidosis and in the absence of other manifestations suggestive of pancreatitis are not of clinical significance.

References and Links

  • Beck, LH. Should the actual or the corrected serum sodium be used to calculate the anion gap in diabetic ketoacidosis? CLEVELAND CLINIC JOURNAL OF MEDICINE  2001; 68 (8) 673-674. (pdf)

Oncology Quandary #004

45 year old woman with metastatic ovarian cancer is admitted for VATS pleurodesis (video-assisted thoracoscopic surgery) and drainage of bilateral pleural effusions.  Her admission chest X-ray is shown below:

image 1 Oncology Quandary #004

During her operation, 2L of fluid is drained from the left chest.  Shortly thereafter, pink frothy sputum starts coming out of the ET tube and the patient markedly desaturates.  The patient is transferred to the intensive care unit and the following chest x-ray is obtained:

image 21 Oncology Quandary #004

Questions

Q1. Describe the chest X-ray.

There is an ET tube, a right IJ central line and bilateral chest drains in situ. There is also ECG monitoring on the patient. Most importantly:

There is near white-out of the left hemi-thorax.

Q2. What is the likely diagnosis?

The history and chest X-ray appearances suggest that the likely diagnosis:

re-expansion pulmonary oedema

Q3. What are the risk factors for this condition developing?

Risk factors include:

  1. long-standing collapse of the lung prior to aspiration
  2. drainage of a large amount of fluid or air over a short period of time
  3. application of suction

Q4. What is Meig’s syndrome?

Meig’s syndrome is the triad of:

  1. ascites,
  2. pleural effusion and
  3. benign ovarian tumor (fibroma)

It resolves after the resection of the tumor. For reasons unknown, the pleural effusion is classically on the right side. This patient has metastatic ovarian cancer with associated pleural effusion so this is not it!

Joe Vincent Meigs, was an American obstetrician and gynaecologist. Meigs was a grandson of Captain Joe Vincent Meigs, who invented an experimental steam monorail known as the Meigs single-track elevated railroad.

image 3 Oncology Quandary #004

Unusual Urine #003

You are looking after a 23 year old male who has a subarachnoid haemorrhage and the nurse calls because the patient has started to pass unusual urine:

image 2 Unusual Urine #003

Questions

Q1. What is the cause of this green urine?

Propofol

Q2. What is the significance of this happening?

This phenomenon usually occurs in the setting of propofol being administered by infusion in at least a moderately high dose. However, it is a benign phenomenon and is not thought to be associated with an increased risk of propofol infusion syndrome or other badness.

Q3. What is the propofol infusion syndrome?

Propofol infusion syndrome (PRIS) is a potentially lethal condition that can occur in patients receiving a propofol infusion at high dose (e.g. >4mg/kg/h) for a prolonged duration (e.g. >29h). It was first described in children but can also occur in critically ill adults and may occur at lower doses.

The criteria for clinically diagnosing PRIS include:

  • Cardiac dysfunction -  especially arrhythmia (such as sudden onset of marked bradycardia resistant to treatment, leading to asystole) and hypotension

and one of:

  • Rhabdomyolysis
  • Acute renal failure
  • Hypertriglyceridemia

Although other features may also be present:

  • Unexplained metabolic acidosis
  • Lactic acidosis
  • Hepatomegaly

The mechanism for PRIS remains obscure as does its true incidence.

Q4. Can the onset of propofol infusion syndrome be predicted?

Routine monitoring for biochemical markers such as serum lactate, creatine kinase, myoglobin, and triglycerides has been advocated for early detection of PRIS. However, even twice-daily evaluations of these laboratory studies – with immediate discontinuation of propofol if derangements are detected – may not be protective. Nevertheless, early discontinuation of propofol may lead to recovery.

The development of a Brugada-like ECG pattern (right bundle branch block with convex-curved ST segment elevation in the right precordial leads) has been noted in some cases of PRIS but the utility of this finding is unclear.

References

ResearchBlogging.org

  • Riker RR, Glisic EK, & Fraser GL (2009). Propofol infusion syndrome: difficult to recognize, difficult to study. Critical care medicine, 37 (12), 3169-70 PMID: 19923937
  • Iyer VN, Hoel R, & Rabinstein AA (2009). Propofol infusion syndrome in patients with refractory status epilepticus: an 11-year clinical experience. Critical care medicine, 37 (12), 3024-30 PMID: 19661801

Pulmonary Puzzle #008

A 3o year old male presents with a 3 day history of fevers and increasing breathlessness.  On presentation he is noted to be severely hypoxic with sats of 80% on room air.  The following chest X-ray is obtained:

image 17 Pulmonary Puzzle #008Questions

Q1. Describe the chest X-ray and outline the differential diagnosis

There are diffuse bilateral pulmonary infiltrates which have a nodular appearance. The differential diagnosis here includes infectious causes such as viral pneumonia and typical and atypical causes of bacterial pneumonia. Non-infectious causes would include hypersensivity pneumonitis and diffuse alveolar haemorrhage. The short history favours an infectious aetiology.

The patient is admitted to the intensive care unit and continues to deteriorate with an increasing oxygen requirement. An arterial blood gas shows a PaO2 of 55 on 15L O2 via a facemask. The respiratory rate rises to the high 40s. Another chest X-ray is obtained:

image 26 Pulmonary Puzzle #008Q2. Describe the chest X-ray now. What would you do next? What problems would you anticipate?

The chest X-ray shows worsening of the previous alveolar infiltrates. The combination of the early rapid progression in the clinical and radiological course combined with the severity of the hypoxia indicates that intubation is required. Non invasive ventilation is not a good option here (except while preparing to intubate) as delaying intubation further here is only likely to make the procedure more dangerous by further limiting the patient’s reserve. The problem that you need to need to anticipate here is rapid desaturation and potential difficulty obtaining adequate oxygenation with bag-mask ventilation if that occurs

Over the following 12 hours the patients condition continues to worsen to the point that the patient is frequently desaturating on 100% oxygen with a PEEP of 18. You are asked to see the patient because the patient has desaturated to 80% on the above settings. The ventilator appears to be working appropriately. On examination, you find the right chest is moving less than the left and there is less air entry on that side.

Q3. What do you do now?

Order a chest X-ray. Even if you are very strongly suspicious that there is a pneumothorax you should not perform needle decompression here. It is likely given the clinical context that the change here represents progression of disease. If there is no pneumothorax and you create one there is a significant risk that the patient will die.   In this case, there was no pneumothorax:

image 3 Pulmonary Puzzle #008

Q4. What are the options for improving oxygenation now?

This patient is failing conventional ventilation. The options for improving oxygenation are:

1. nitric oxide

2. prone ventilation

3. inverse ratio ventilation

4. ECMO

5. High Frequency Jet Ventilation

A non-conventional ventilation strategy is employed and the following chest X-ray is obtained:

image 4 Pulmonary Puzzle #008

Q5. Describe the chest X-ray.

This x-ray shows an ECMO cannula inserted via the right internal jugular route. With this particular cannula, venous blood is taken from the superior vena cava and the inferior vena cava. It is then oxygenated and the cannula has a third lumen which allows arterialised blood to be directed towards the tricuspid valve in the right atrium under TOE guidance.

On ECMO things got worse…

image 18 Pulmonary Puzzle #008

and then they got better…
image 6 Pulmonary Puzzle #008

Q6. Describe the most recent chest x-ray.

The chest x-ray has dramatically improved. However, there is a small right basal pneumothorax.

Metabolic Muddle #003

An 87 year old female presented with a subarachnoid haemorrhage.  GCS 8/15.  A nasogastric tube was unable to be placed due to patient agitation.  As a consequence, the patient was fasted for five days due to concern about swallowing.   Subsequently, an arterial blood gas was obtained:

image 14 Metabolic Muddle #003

Questions

Q1. Describe the arterial blood gas

  1. There is a metabolic acidosis with a high anion gap (HAGMA).
  2. The bicarbonate has decreased by more than the anion gap has increased which is due to a coexistent normal anion gap acidosis (NAGMA).
  3. There is a respiratory alkalosis. The pCO2 of 12mmHg is much lower than the respiratory compensation you would expect with this degree of metabolic acidosis (expected pCO2 = 1.5 * HCO3 +8 = 25 ).

The combination of these three abnormalities has led to relatively normal pH despite severe acid-base disturbance.

Q2. What are the causes of metabolic acidosis with raised anion gap and what is the likely cause here?

There are two ways of remembering this.

The easy way is to remember ‘left total knee replacement’:

Lactate
Toxins
Ketones
Renal Failure

The more complicated way is CAT-MUDPILES:

Cyanide, Carbon monoxide
Alcoholic ketoacidosis
Toluene
Methanol, metformin
Uraemia
Diabetic Ketoacidosis
Phenformin, pyroglutamic acidosis, propylene glycol, paracetamol
Isoniazid, Iron
Lactic acidosis (many causes)
Ethanol, Ethylene glycol
Starvation, salicylates

The history suggests starvation ketoacidosis. There were ketones in the urine confirming this diagnosis.

Q3. What are the causes of normal anion gap acidosis and what is the likely cause here?

The easy way to remember is OGRe:image 24 Metabolic Muddle #003

Others (eg chloride)
GI loss
Renal loss

The more difficult way is to remember is USED CARP (the A and the R can be reversed – this is optional):

Ureteroenterostomy
Small bowel fistula
Extra Chloride
Diarrhoea
Carbonic anhydase inhibitors
Addisons disease
Renal tubular acidosis
Pancreatic fistula

Neurosurgeons like to give everyone lots of normal saline. The chloride is high. The likely diagnosis is hyperchloraemic metabolic acidosis secondary to normal saline.

ENT Equivocation #001

A 38 year old male with a background history of type 2 diabetes presents with fevers, rigors and pain on swallowing. There is no sign of impending airway compromise; however, marked trismus is noted. The following plain X-ray is obtained:

image 13 ENT Equivocation #001

Questions

Q1. What is the diagnosis?

there is gross soft tissue swelling evident anterior to the vertebral bodies. The likely diagnosis is retropharngeal abscess

Q2. What radiological investigation is indicated now?

A CT neck will allow you to determine the extent of the collection and whether it is amenable to drainage

image 21 ENT Equivocation #001

Q3. Describe the CT scan

There is an area of hypodensity in the right posterior pharynx consistent with an abscess.

Q4. The chest X-ray is normal but the ENT surgeon requests a CT chest. What do you think the purpose of this investigation is?

A CT chest is indicated to exclude unappreciated mediastinal mischief due to descending mediastinitis. This is a rare but highly lethal complication.

Q5. What is Lemierre’s syndrome?

Lemierre’s syndrome is characterised by disseminated abscesses and thrombophlebitis of the internal jugular vein after infection of the oropharynx. The predominant pathogen is a gram-negative anaerobic bacillus, Fusobacterium necrophorum.

Pulmonary Puzzle #007

A 67 year old gentleman with a BMI of 45 was waiting for his respiratory outpatient clinic appointment.  While waiting, he fell asleep.  A medical emergency was called because he could not be woken up.  On arrival of the MET team the patient is found to have a blood pressure of 140/70, a heart rate of 100bpm and oxygen sats of 68% on room air.  He is breathing spontaneously but requires airway support.  His  GCS is 3/15.  Supplemental oxygen is applied and the following arterial blood gas is obtained.

image 1 Pulmonary Puzzle #007

Questions

Q1. Describe the arterial blood gas?

There is a moderately severe acidaemia due to severe respiratory acidosis. There is a marked metabolic alkalosis which indicates that there is likely to be severe underlying hypercapnic respiratory failure. The oxygen saturation is 97%.

Q2. If the baseline bicarbonate is 46, what is the baseline CO2?

In a chronic respiratory acidosis the bicarb rises by 4 for every 10mmHg rise in the CO2. So, a bicarb of 20 above normal corresponds to a CO2 of 50 above normal. In other words, the baseline CO2 would be about 90mmHg!

Q3. Is supplemental oxygen a good idea in this case?

Yes. Without supplemental oxygen, a CO2 of 132mmHg is not compatable with life. Calculating the PAO2 from the alveolar gas equation for a patient on room air demonstrates this:

image 2 Pulmonary Puzzle #007
While supplemental oxygen may precipitate worsening type 2 respiratory failure in patients with chronic hypercapnia, removing supplemental oxygen in the setting of such extreme hypercapnia will precipitate death.

Renal Riddle #001

Consider a 65 year-old male presenting with right-sided flank pain radiating to the groin.  The following CT scan was taken to confirm a presumed diagnosis of renal colic:

image 114 Renal Riddle #001

image 210 Renal Riddle #001

Questions

Q1.  Describe the CT scan

CT scan is non-contrast; however, there is:

  • right-sided retroperitoneal blood evident.
  • an abdominal aortic aneurysm.

It is important to remember that the commonest cause of the ‘classic’ presentation of renal colic amongst patients presenting to have a post-mortem is ruptured abdominal aortic aneurysm.

This patient needs an emergency AAA repair.

The patient was taken to theatre for emergency surgery.
The following biochemistry results were taken post-operatively:

image 37 Renal Riddle #001

Q2.  Describe the biochemistry.  What diagnosis is suggested by these biochemical findings?

Biochemistry demonstrates acute renal failure with a reduced urea-to-creatinine ratio.

The likely diagnosis is rhabomyolysis in this clinical context. Features suggestive of this diagnosis are:

  • increased urea and creatinine with a reduced urea-to-creatinine ratio
  • hyperphosphataemia, hypocalcaemia, hyperkalaemia
  • metabolic acidosis
  • increased CK (usually to greater than 40,000)
  • Although not measured here, AST, and LDH are also increased in rhabdomyolysis

Q3.  What are the other potential causes of renal failure to consider in this clinical situation?

  1. hypovolaemia from bleeding
  2. renal artery occlusion during operation
  3. use of contrast in pre-operative CT scan (not in this case)
  4. use of nephrotoxic drugs like gentamicin
  5. low cardiac output from peri-operative myocardial infarction
  6. abdominal compartment syndrome

Pulmonary Puzzle #005

A 17 year old female with a background history of HIV presents with a 3 day history of fevers, chills and rigors.  Her admission chest X-rays are shown below:

image 112 Pulmonary Puzzle #005

image 29 Pulmonary Puzzle #005

Questions

Q1. Describe the chest X-ray.

The chest X-ray shows dense consolidation of the right middle lobe.

The radiographic features of lobar consolidation are:

  • homogeneous opacification.
  • minimal volume loss.
  • air bronchograms and air alveolograms (lucent areas due to air-filled acini).
  • sharp border where the infiltrate abuts an interlobar fissure.
  • silhouette sign – loss of the right heart border on the AP film indicates that the right middle lobe is involved; this occurs because of obliteration of the normal interface between lung air and mediastinal tissue/fluid.
  • obliteration of normal vascular markings.

Q2. What is the most likely diagnosis?

The commonest cause of pneumonia in patients with HIV is pneumococcal pneumonia. The clinical history and radiological features are consistent with this diagnosis.

Q3. A decision is made to perform a diagnostic bronchoscopy. Where will you aim the bronchoscope?

The plain chest x-ray demonstrates consolidation of the right middle lobe so you should aim the bronchoscope down the bronchus intermedius from the right main brochus towards this lobe.

image 36 Pulmonary Puzzle #005

Segments of the right lung

Q4. How do you navigate your way to the right middle lobe?

You practice!

Bronchoscopy International is a fantastic learning resource for learning endobronchial anatomy.

NB: The Step-by-Step presentation is optimised for use on Microsoft internet Explorer and works well in Safari, but looks like a pig’s breakfast in Firefox!

The following video, which is one of many at the site, demonstrates how to get from the right main bronchus to the bronchus intermedius:

embedded by Embedded Video

From the distal bronchus intermedius the bronchoscope can then access the segments of the right middle lobe (RB4 and RB5) as well as the superior segment of the right lower lobe (RB6).

Oncology Quandary #001

Consider a 16 year old who presents with a 3 week history of severe hip pain followed by increasing breathlessness and left sided chest pain. His admission chest X-ray is shown below:

image 111 Oncology Quandary #001

A biopsy is performed on a left hip lesion which reveal a small blue round cell tumour

A number of days later the following chest x-ray is obtained:

image 27 Oncology Quandary #001

Questions

Q1. What are the potential causes of unilateral ‘white-out’ of a hemithorax?

  1. pleural fluid e.g. hemothorax, chylothorax, pleural effusion.
  2. complete collapse of one lung (e.g. due to obstruction of a main bronchus)
  3. dense consolidation of one lung
  4. an entire hemithorax full of cancer

In this case the entire hemithorax is filled with cancer. A CT of the chest shows the tumour mass.

image 35 Oncology Quandary #001

The advice of the Medical Oncologist is that this tumour may respond to chemotherapy and there is a good chance of cure; however, it may take a week or more for the patient to respond to treatment. The patient is admitted to the Intensive Care Unit and symptoms of breathlessness continue to worsen.

Q2. How will you manage this?

This a big problem.

The chest X-ray reveals that the right lung is not aerated and the left main bronchus is significantly narrowed. Progressive breathlessness may indicate that the tumour is continuing to expand. Intubation is not likely to improve the situation if this is the case and, if the patient is up to it, you may need to have a difficult conversation about limitations of therapy.

If the patient is going to be intubated, the risk of death around the time of intubation is significant as you may not be able to ventilate the patient. In addition, the CT scan reveals that the tumour is compressing the right ventricle. The risk of haemodynamic embarrassment at the time of  intubation is significant. The patient, the patient’s family and staff need to know that the patient is likely to die around the time of intubation.

Metabolic Muddle #002

A 50 year old Chinese female presents with severe weakness.  She has a history of previous similar episodes that self-resolved.

This is her admission ECG:

image 110 Metabolic Muddle #002

ECG of a patient with recurrent weakness (click to enlarge)

Questions

Q1. Describe the ECG.

The ECG demonstrates

  • sinus rhythm with a rate of 70bpm
  • Normal axis
  • Flattened T waves with the presence of U waves.
  • Normal QTc (Corrected QT)

Q2. What is the likely diagnosis?

Hypokalaemic periodic paralysis – this patient had a potassium of 1.9mmol/L.

Q3. How is this condition treated?

During an acute attack treatment involves correction of hypokalaemia with potassium supplementation.

For prophylaxis, patients are usually treated with acetazolamide.

Q4. Why is it important to measure the thyroid function?

The major differential here is thyrotoxic periodic paralysis.

Thyrotoxic periodic paralysis also causes periodic paralysis associated with hypokalaemia. Interestingly, the prevalence of thyrotoxic periodic paralysis in patients with thyrotoxicosis is estimated to be 0.1-0.2% in Caucasians and 13-14% in Chinese.

Trauma Tribulation #004

A 21 year-old female presents with acute onset of unrelenting abdominal pain and vomiting four years after a major motor vehicle accident.  A chest X-ray is performed:

image 19 Trauma Tribulation #004

Questions

Q1. What is the likely diagnosis?

Traumatic rupture of the diaphragm with strangulation of viscera in the chest. Ambroise Paré, in 1579, described the first case of diaphragmatic rupture diagnosed at autopsy. The patient was a French artillery captain who initially survived a gunshot wound of the abdomen, but died 8 months later of a strangulated gangrenous colon, herniated through a small diaphragmatic defect that would admit only the tip of the small finger.

Q2. How could this complication have been prevented?

The only answer I can think of to this question is to have made the diagnosis earlier and repaired the diaphragm!  However, traumatic rupture of the diaphragm is a difficult diagnosis to make.   A high index of suspicion is required.

Pathognomonic chest X-ray findings include:

  • the presence of bowel or stomach gas in the chest
  • a nasogastric tube that passes through or finishes in the chest

Suggestive chest X-ray findings include:

  • Irregularity of the diaphragmatic outline
  • an elevated hemidiaphragm
  • Mediastinal shift without pulmonary or intrapleural cause

Q3.  How is this condition treated?

Treatment requires surgical repair of the diaphragm.  In this case, resection of strangulated viscera may be required.  Laparotomy is the preferred approach in acute cases because it allows for treatment of associated abdominal injuries while thoracotomy is the best approach in chronic cases.

Pulmonary Puzzle #004

Consider a 56 year old male with no past medical history presenting with 10 days of fevers, chills, myalgias and cough followed by worsening breathlessness over the past 4 days.  His admission chest X-ray is shown below:

image 18 Pulmonary Puzzle #004

Questions

Q1.  Describe the chest X-ray findings:

The chest X-ray demonstrates a dense alveolar infiltrate involving the lateral aspect of the left mid-zone.

The patient rapidly deteriorated with fulminant shock, multiorgan failure and worsening oxygenation.  The following chest ray is taken shortly after ICU admission

image 26 Pulmonary Puzzle #004

Q2. What devices are present on the chest X-ray?

  1. right IJ central line
  2. left IJ vascath (dialysis catheter)
  3. nasogastric tube
  4. endotracheal tube

Q3.  Which device is in the wrong place and where should it be?

The left IJ vascath is in too far.  Central lines and vascaths should not be inserted beyond the superior extent of the pericardial reflection (which corresponds to the take off of the right main bronchus) because beyond this point they can erode through the superior vena cava or the right atrium / ventricle leading to pericardial tamponade and death

A subsequent chest X-ray is as follows:

 Pulmonary Puzzle #004

Q4. What has happened since the previous chest x-ray?

A chest drain has been inserted draining the left pleural effusion and the vascath has been pulled back to an appropriate position.

The following microbiology is obtained:

Microbiology SpecimenDescription
Respiratory SputumLiquid, blood stained
Moderate growth of normal URT flora
Heavy growth of Streptococcus pyogenes
Blood CultureSpecimen: Venous
Growth of Gram positive cocci resembling streptococci in aerobic bottle after 1 day.
Isolate identified as Streptococcus pyogenes

Q5.  What is the diagnosis?

The overwhelming evidence here points to a diagnosis of S. pyogenes pneumonia, bacteraemia and empyema!  The clinical history suggests the possibility of a bacterial infection complicating influenza and, indeed, this turned out to be the case:

 Pulmonary Puzzle #004

Influenza may predispose to invasive group A Strep disease (at least it does in mice)

Q6.  What is the prognosis?

In a series of 2079 cases .of invasive group A Strep infection, the case fatality rate was 38% for pneumonia, compared with 26% for patients with necrotizing fasciitis.

Laboratory Tester #002

A 72 year old female is admitted following an emergency abdominal aortic aneurysm repair.  The day after her surgery, the following biochemistry results are obtained:

MarkerResultUnitsNormal Range
Sodium136mmol/L[138-146]
Potassium6.4mmol/L[3.5-4.9]
Urea8.9mmol/L[3-7.3]
Creatinine211µmol/L[62-103]
Magnesium1.05mmol/L[0.76-0.99]
Calcium1.12mmol/L[2.25-2.49]
Calcium (Corrected)1.74mmol/L[2.25-2.49]
Phosphate3.67mmol/L[0.95-1.6]
Albumin9g/L[34-46]

Questions

Q1: Describe the biochemical findings

Beyond the obvious (i.e. every value that fall outside of the reference range), the urea to creatinine ratio is low.  The expected creatinine based on the urea of 8.9 is approximately 89.  Whereas, the actual creatinine is 211.

Q2:  What are the causes of a reduced urea to creatinine ratio?

The causes of reduced urea to creatinine ratio are as follows:

  1. Low protein diet
  2. Malnutrition
  3. SIADH
  4. Pregnancy
  5. Severe Liver Dysfunction
  6. Rhabdomyolysis

Q3:  What is the likely diagnosis in this case?

Rhabdomyolysis.  The diagnosis is effectively confirmed by a urine dipstick and urine microscopy:  Myoglobinuria can be inferred if a urinary dipstick is positive for blood when there are no red cells in the urine sediment.  This is because, the dipstick test is unable to distinguish between myoglobin and haemoglobin.

Q4:  How is this condition managed?

The management of rhabdomyolysis was recently reviewed in a clinical vignette in the New England Journal of Medicine. The recommendations in this review were as follows:

  1. aggressively correct hypovolaemia (a common problem due to sequestration of fluid in muscle)
  2. target a urine output of 3ml/kg/hr
  3. monitor serum potassium closely and treat hyperkalaemia with standard measures
  4. alternate each litre of saline with 1L litre of D5W plus 100mmol of bicarbonate if the urine pH is less than 6.5 (they suggest abandoning urinary alkalinisation if the urine pH does not rise after 4-6 hours of treatment or if symptomatic hypocalaemia develops)
  5. consider treatment with mannitol in a dose of up to 200g per day with a total accumulated dose of no more than 800g.  Mannitol has dual roles of flushing nephrotoxic agents through the renal tubules and reducing muscle compartment pressures.  They suggest that mannitol diuresis be abandoned if diuresis of >20ml/hr is not achieved or if the osmolar gap rises above 55mOsm/kg.
  6. commence renal replacement if there is treatment-resistant hyperkalaemia, a rapidly rising potassium, volume overload or a metabolic acidosis with a pH <7.1.

It is important to emphasise that the quality of evidence to guide treatment is very poor.  Urinary alkalinisation and mannitol have a firm pathophysiological basis but no trial has demonstrated any particular benefit from either of these therapies.

The urine looks like this:

image 34 Laboratory Tester #002

In this case, the cause of this is myoglobinuria.

Q4:  What are the other causes of urine that looks like this?

  1. Haemoglobinuria
  2. Porphyria
  3. Bile pigments
  4. Food and drugs (levodopa, metronidazole, nitrofurantoin, iron, chloroquine and methyldopa all cause brown urine)

Cardiovascular Curveball #002

You are managing a 56 year old woman with severe pneumonia in the Intensive Care Unit when you are called to see her because her leg has suddenly turned blue:

image 16 Cardiovascular Curveball #002

Questions

Q1: What is the diagnosis?

 Phlegmasia Cerulea Dolens

Less frequent manifestations of venous thrombosis include phlegmasia alba dolens, phlegmasia cerulea dolens, and venous gangrene. These form a clinical spectrum of the same disorder. All 3 manifestations result from acute massive venous thrombosis and obstruction of the venous drainage of an extremity.  In phlegmasia alba dolens, the thrombosis involves only major deep venous channels of the extremity, therefore sparing collateral veins. The venous drainage is decreased but still present; the lack of venous congestion differentiates this entity from phlegmasia cerulea dolens.

Q2:  What are the complications?

1. Pulmonary embolism

2. Venous Infarction of the limb

3. Fluid sequestration in the limb and systemic inflammatory response syndrome leading to hypotension

Q3:  How is this condition managed?

This a rare condition and the management is evolving.  Traditional treatment consists of standard anticoagulation; however, increasingly, invasive therapies such as catheter directed thrombolysis, surgical thrombectomy and systemic thrombolysis are employed in these patients

Top 10 Rules of Expensive Scare Medicine

  1. Coagulopathy does not cause you to bleed precipitously from a single drain; this is an indication for a re-inspection of surgical excellence.
  2. A patient with a worsening metabolic acidosis after damage control laparotomy is usually still bleeding
  3. If you think that a patient who has had an abdominal aortic aneurysm repair might have dead gut then they do
  4. If you measure something and it is not normal, make it normal if it is safe to do so.
  5. Penicillin, flucloxacillin, cephazolin  and vancomycin is not a good combination for antibiotic prophylaxis even if the surgeon suggests it.
  6. If the surgeon says that a septic patient is too sick for an operation there are only two possibilities:
    1. the surgeon is wrong
    2. the patient is dead
  7. Usually if you ask an Oncologist how long a patient with a metastatic cancer who has exhausted all treatment options is going to live, they will tell you ‘one year’.  This is an ‘oncologist year’.  In order to work out the patient’s actual life expectancy, you should begin by halving the number of days in a year  (giving you a figure of approximately 182) and then you should subtract the patient’s age.  If the patient is currently admitted to the intensive care unit, you should subtract 10 for every organ system that has failed.   This figure will give you the patient’s life expectancy.  For patients outside the intensive care unit, this figure is in days.  For patients in the intensive care unit, this figure is in hours.
  8. If a patient who has had a bone marrow transplant is admitted to an intensive care unit they are in big trouble and when they engraft it does not mean they are getting better.
  9. Neurosurgeons like doing operations.  If a  patient achieves flexion this is a good outcome.
  10. Every patient you ever treat is going to die; if they are 85,  it is likely to be sometime soon.

Laboratory tester #001

76 year old male living alone. Found obtunded at home by neighbours. Breathing rapidly and muttering incoherently. No other history available. Admission arterial blood gas shown (note that despite the labelling this specimen is arterial):

image 15 Laboratory tester #001

Questions

Q1:  Describe the arterial blood gas results

The first step:  is the patient acidaemic or alkalaemic?

there is severe acidaemia

The second step:  is there a metabolic acidosis or a respiratory acidosis or both?

there is a severe metabolic acidosis

The third step:  is there appropriate compensation?

The estimated expected CO2 is 1.5xHCO3 + 8 i.e. approximately 13 so its pretty close

The fourth step:  what is the nature of the metabolic acidosis?

The anion gap is markedly elevated at 35 [(Na+ K+) - (Cl-+HCO3-)]

The fifth step:  is there a coexistent normal anion gap acidosis or pre-existing metabolic alkalosis?

If the raised anion gap acidosis is the only metabolic disturbance, the bicarbonate drops by the same degree that the anion gap rises.  In this case, assuming a normal anion gap of 12, the anion gap has increased by 23 while the HCO3- has decreased by 23.   Assuming a normal HCO3- of 26 the bicarbonate has decreased by 23 to finish up at 3.  So the raised anion gap acidosis is the only metabolic disturbance.

If the bicarbonate drops less than anticipated, it must have started off at a higher level than you normally expect (i.e. there must be a pre-existing metabolic alkalosis)

If the bicarbonate drops more than anticipated, there must be another source of acidosis (i.e. a co-existent normal anion gap acidosis)

confused yet?

The final step:  summarise

There is a severe raised anion gap metabolic acidosis with appropriate respiratory compensation 

 Q2:  What are the causes of metabolic acidosis with raised anion gap?

The simple way of remembering is to remember only four:

Lactate

Toxins

Ketones

Renal failure

LTKR (left total knee replacement)

The complicated way is to remember MUDPILES

Methanol, metformin

Uraemia

Diabetic ketoacidosis

Phenformin, pyroglutamic acid

Iron, isoniazid

Lactate

Ethanol, ethylene glycol

Salicylates

 In this case the cause was renal failure:

image 25 Laboratory tester #001

Microbial Mystery #002

Consider the following scenario:

A 27 year old female with metastatic ovarian cancer for whom curative options have been exhausted arrives in the emergency department in extremis.   Her history is of rapid onset (over a few hours) of shortness of breath, high fevers and rigors. Her vital signs on arrival in the emergency department are as follows HR of 190, BP 80/30, RR of 65, temperature of 39 and saturations of 90% on 10L via face mask.

Questions

Q1. Outline your management?

This patient is critically unwell and requires immediate assessment and resuscitation in an appropriately monitored environment.  A team approach will be required and initial management should be directed towards establishing adequate airway, and stabilising breathing and circulation. 

On the face of things this sounds bad.  In a patient with metastatic cancer in whom all curative options have been exhausted it is necessary to weigh the burden of invasive treatment against the potential benefits; however, unless you can rapidly gain information from the patient, the patient’s family or someone else regarding limitations of therapy, it is better to address the immediate crisis now then ask questions later (in my view)

 

Shortly after arrival the patient is intubated.   Her first chest X-ray is taken after intubation
  
image 14 Microbial Mystery #002
 
Q2. Describe the chest X-ray.

This chest X-ray shows an endotracheal tube in appropriate position and a nasogastric tube in appropriate position.  There are diffuse bilateral pulmonary infiltrates with air bronchograms visible.
  
The following blood test results are obtained:
  
image 24 Microbial Mystery #002 
Q3. What is the likely diagnosis?

The history and investigations strongly suggest that this patient has fulminant bacterial pneumonia with associated septic shock.

Q4. What are the likely causative pathogens and what empirical antibiotics would you use?

This picture of very rapid onset is typically seen with Pneumococcal pneumonia and Staph. pneumonia.   It may also occur with Strep. pyogenes pneumonia but this is a relatively rare condition.  Empirical antibiotics will vary according to local susceptibilities; however should cover Pneumococcus (eg 2nd or 3rd generation cephalosporin) and Staph. including community acquired MRSA (eg clindamycin if local susceptibilities allow or linezolid or vancomycin).   I would also cover atypical organisms with a macrolide in the first instance.

In this case, the diagnosis of Pneumococcal pneumonia was confirmed by a positive urinary Pneumococcal antigen:

 

image 33 Microbial Mystery #002
This patient had rapidly worsening shock and deteriorating respiratory and renal function over the first 8 hours of hospital admission; however, she rapidly recovered.   She was extubated within 24 hours and inotropic support was rapidly weaned.   She was discharged from hospital 72 hours after admission.   A useful point here is that a patient with very rapid onset of severe  bacterial infection  who receives very rapid appropriate antibiotics can recovery rapidly.

Cardiovascular Curveball #001

This 86 year-old male presented with shortness of breath.  He developed a complication after  insertion of a left chest drain.

This CT scan demonstrates that complication:

image 22 Cardiovascular Curveball #001

Questions

Q1. What is the complication?

the chest drain is in the left ventricle.

Q2. Outline your management.

This complication was identified at the time by the presence of pulsatile bright red blood coming from the drain.
  • Clamping the drain to prevent exsanguination is a good first step!
  • Not taking the drain out is a good second step.
  • The next step is to prepare the patient for cardiac surgery to remove the drain and repair the heart.  In this patient, removing the drain and repairing the heart was achieved via a mini thoractomy.
In addition to the issues of patient care, this is a sentinel event and appropriate reporting and follow-up needs to be undertaken. The CT below demonstrates how this complication arose…not everything that looks like a left pleural effusion on a plain chest X-ray is one!
image 13 Cardiovascular Curveball #001
Q3. How could this complication have been prevented?

Put your finger in the hole!

One of the most important steps in the insertion of an intercostal catheter is to insert a finger through the hole you have just made. Do this before inserting the intercostal catheter.

Using your finger you can detect any adhesions that may lead to penetration of the lung on insertion of the intercostal catheter, as well as the presence of underlying organs such as a beating heart!

In this case, the intercostal catheter is a one from a Seldinger kit. If you are going to use one of these kits, you should do an ultrasound to make sure that there really is a pleural effusion that can be safely drained.