The INR is high, the APPT is high and the fibrinogen is very low.

These results are consistent with disseminated intravascular coagulation (DIC).

In severe DIC there are fragmented red blood cells (schistocytes).

In this case, potential pregnancy-related causes of DIC include:

1. amniotic fluid embolism
2. pre-eclampsia
3. HELLP syndrome
4. post-partum haemorrhage

The fact that bleeding did not occur at the time of the caesarian section suggests that the problem has developed subsequently making amniotic fluid embolism the most likely diagnosis.

Other pregnancy-related causes of DIC (not relevant here) include:

1. placental abruption
2. septic abortion
3. intrauterine death

The most important non-pregnancy related cause of DIC that needs to be considered in this scenario is:

1. severe sepsis

It turns out that knowing one thing about the coagulation cascade is useful:

That one thing is that conversion of fibrinogen to fibrin is at the bottom of the cascade. That means that if the fibrinogen is low, the patient will not form clot until they get cryoprecipitate.

Any patient with a coagulopathy who has a low fibrinogen should have their fibrinogen corrected as the first priority.

The usual dose of cryoprecipitate is one unit of cryoprecipiate per 30 kg of body weight. In this case, the fibrinogen level is exceptionally low and administration of a greater dose than this would be appropriate. The patient should also receive fresh frozen plasma and may require platelets (depending on the platelet count).

There is extensive air space change involving the right middle and lower zones and the left lower zone.  There is loss of volume in the right side of the chest consistent with previous surgery.  Given the history, the findings are suggestive of severe pneumonia.

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The oxygen saturation and the PaO2 are low. The patient is acidaemic and there is a respiratory acidosis.

The expected HCO3 if this was an acute disorder would be approximately 30 (HCO3 increases by 1 for every 10mmHg increase in CO2 for an acute disorder).  However, the actual bicarbonate is higher than this.  If the change in CO2 was all chronic the expected HCO3 would increase by 4 for every 10mmHg increase in CO2 i.e. a bicarbonate of approximately 40 would be expected. The bicarbonate is actually about half way between these two predicted values.

This is consistent with acute-on-chronic type 2 respiratory failure.

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The patient is intubated and lined.  The consolidation is worse.

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This is a complicated question.

The serum concentrations of penicillin that can be achieved with intravenous therapy are greater than the MIC even for highly resistant pneumococci and penicillin penetrates lung tissue very well (this is not the case for meningitis where relatively poor CNS penetration may limit the effectiveness of penicillin).

In a prospective study of children with community acquired pneumococcal infections due to pneumococcus treated with penicillin, there was no difference in mortality based on whether pneumococci were penicillin-resistant or penicillin-sensitive.  However, in this and other studies, the number of patients with an MIC of >4mcg/ml is very small.  It is not known whether highly active beta lactams such as ceftriaxone are more rapidly efficacious than penicillin for highly resistant strains — this simply has not been studied.

The key issues are probably dose and MIC.

Giachetto et al (2004) reported adequate interdose time serum concentrations of greater than 4mcg/ml using 200 000 units/kg/day.  So, in summary if the MIC is 2mcg/ml or less there are prospective data that suggest that standard dose penicillin is just fine.  If the MIC is more than 2mcg/ml there are no prospective data that support use of penicillin; however, provided that a high dose of penicillin is used, penicillin is likely to be effective — although, using an alternative beta lactam is this setting would be reasonable.

• The first step: is the patient acidaemic or alkalaemic?

• There is significant acidaemia

• There is a severe metabolic acidosis

• The estimated expected CO2 is 1.5xHCO3 + 8 i.e. expected CO2 is 24 (so similar to actual CO2 of 27)

• The anion gap is elevated at 25 [(Na+ K+) - (Cl-+HCO3-)]

• The anion gap is 11 above normal while the the bicarbonate is 13 below normal. There is a minor contribution to the acidosis due to a normal anion gap acidosis. In this case, the normal anion gap acidosis is hyperchloraemic (chloride is elevated).

• There is a severe raised anion gap metabolic acidosis which is predominantly due to raised lactate. Of note, there is a raised lactate associated with a low glucose.

1. overwhelming sepsis
2. liver failure
3. beta blocker overdose

The biochemistry reveals the following:

Bilirubin 63 (4-22)
ALP 184 (36-100)
ALT 5003 (12-48)
Protein 47 (66-83)
Albumin 27 (38-48)

Fulminant hepatic failure

1. paracetamol overdose
2. idiosyncratic drug reactions
3. hepatitis A
4. hepatitis B
5. ischaemic hepatitis
6. autoimmune hepatitis
7. Wilson’s disease
8. Budd Chiari syndrome
9. Acute fatty liver of pregnancy

Acute hepatitis with jaundice and coagulopathy without hepatic encephalopathy is referred to as severe acute hepatitis.  Fulminant hepatic failure is defined as the appearance of hepatic encephalopathy in a patient with acute deterioration of liver function with no previous history of liver disease.

There is collapse of the left upper lobe, the right middle lobe and the right lower lobe.

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Deoxygenated blood is being shunted through the collapsed areas of lung. This shunted blood is not exposed to the oxygen that the patient is breathing in.

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This has happened because the patient is unable to cough (he is paralysed) and the left upper lobe bronchus and bronchus intermedius are blocked with sputum plugs.

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The options are to:

(i) perform a bronchoscopy and remove the plugs
(ii) attempt to reinflate the lungs using recruitment manoeuvres

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One commonly described technique is to apply 40cmH20 of PEEP for 40 seconds. This technique is often poorly tolerated for two reasons. Firstly, during the manoeuvre, the size of West Zone 1 is increased and the patient often desaturates as a consequence of this. Secondly, the prolonged application of high PEEP significantly reduces venous return and significant hypotension often results.

An alternative method is to change the patient to a pressure controlled mode of ventilation, to increase the PEEP to 20cmH20 and then to apply Pressure Control at 20-30cmH20 above PEEP for 5 breaths. This method is generally better haemodynamically tolerated and provides effective recruitment.

Complications of recruitment maneuvers include:

• pneumothorax
• hypotension
• hypoxia
• raised intracranial pressure

The chest X-ray shows resolution of the left upper lobe collapse. The right middle and lower lobe collapse is persistent.

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It depends on the clinical condition of the patient.

The intervention that is likely to be required to improve the right sided collapse is a bronchoscopy; however, given that the patient has raised intracranial pressure, this is may be poorly tolerated.

In this instance a bronchoscopy was able to be safely performed and the following chest X-ray showing improved expansion of the right base was obtained after the procedure:

The CTA chest reveals the presence of a thoracic aortic dissection

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There are two systems in common usage.

The DeBakey Classification:

• type 1 involves the ascending aorta only
• type 2 involves the ascending and descending aorta
• type 3 involves the descending aorta only

The Stanford Classification:

• type A is any dissection that involves the ascending aorta
  type B is any dissection does not involve the ascending aorta

Michael DeBakey (1908-2008)

At the age of 97, Michael DeBakey – who we met briefly in SurgeXperiences 318 – suffered an aortic dissection. He declined surgery (the procedure that he had developed); however, after he lapsed into unconsciousness, the surgery was performed anyway with the approval of the local hospital ethics committee. He was hospitalised for 8 months after his operation but eventually recovered and was able to return to work. He subsequently thanked the surgical team for prolonging his life and worked until the day he died at the age of 99.

A car mechanic said argumentatively to his client, a cardiac surgeon: “So Doc, look at this work. I also take valves out, grind ’em, put in new parts, and when I finish this baby will purr like a kitten. So how come you get the big bucks, when you and me are doing basically the same work?” The surgeon replied: “Try doing your work with the engine running.”
— legend has it the surgeon was Michael DeBakey (1908–2008)

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Type A dissections are usually managed surgically with aortic root replacement. Type B dissections are usually managed with endoluminal approaches and medical management.

While awaiting definitive intervention, blood pressure control is the most critical intervention. Blood pressure should be controlled as rapidly as possible aiming for a systolic blood pressure of 120mmHg or even less using a combination of IV beta blocker and GTN +/- sodium nitroprusside. Where it is available IV labetatolol is a good choice.

Aortic dissection has a mortality of at least 1% per hour for the first 48 hours and 80% of patients die because of aortic rupture or cardiac tamponade. Stringent blood pressure control reduces mortality considerably and should be given high priority.

The most significant finding on this ECG is the presence of electrical alternans. The rhythm is sinus tachycardia at 100/min and the axis is normal.

The investigation indicated is an echocardiogram to confirm the presence of a pericardial effusion and to look for echocardiographic evidence of  pericardial tamponade.

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Pulsus paradoxus is defined as an inspiratory drop in blood pressure of 10mmHg or more during normal breathing.

It is caused by:

1. pericardial tamponade
2. hypovolaemia (especially during positive pressure ventilation)
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.

Check that the R-R interval on the ECG is regular to rule out arhymthmia as the cause of a fluctuating systolic blood pressure.

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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

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

Diabetic ketoacidosis

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.

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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.

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

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

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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.

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

re-expansion pulmonary oedema

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

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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.