ABG Analysis Case 4

Answer the questions at the bottom of the page when all data has been reviewed

History & Examination

An elderly Jamaican couple, both in their 70s, attend ED/ER. The gentleman is concerned about his wife. She had attended her GP (family physician) with abdominal pain earlier that day and on the basis of a urinalysis result (see below) had been diagnosed with a UTI. She had a history of culture-positive UTIs over recent years. On this occasion, her GP had started her on oral antibiotics to which she had responded in the past. The abdominal pain was diffuse and worsened in the hours after she went home from the GPs surgery. In that time, she also developed nausea and vomiting. She was not able to keep any fluids down and a concerned neighbour had called an ambulance. The couple had met shortly after migrating to Britain in the early 1950’s. Due to their humility, the history is difficult to obtain. They avoid eye contact, are softly spoken and answer all questions with ‘yes doctor’ or ‘no doctor’. On closer questioning the patient confirms that her abdominal pain has become ‘very bad’ over the course of the day. She had opened her bowels that day. The bowel movement was loose but she had not noticed any blood.

On examination, there is no abdominal distention. The abdomen is soft with some mild epigastric tenderness on palpation. There is no rebound tenderness or guarding. Bowel sounds are present and of normal intensity. There are some minor inspiratory crepitations at the right lung base.

Urinalysis result (obtained from GP)

Nitrites: negative

Leukocytes: ++

Blood: +

Investigations

10 VBG Bowel infarction Csi

Flut CSi

AXR: normal

CXR: a degree of cardiomegaly. Nil else.

Observations

J couple

 

j fluids


Questions

Q1. What abnormalities are present on her initial hospital investigations?

Q2. Can you offer a differential diagnosis?

Q3. What additional investigations should be carried out?

Q4. Given the diagnosis established in Q3, what are the therapeutic options?

Q5. What do you make of the original diagnosis of UTI?


Answers

Q1. What abnormalities are present on her initial hospital investigations?

VBG

10 VBG Bowel infarction Csi

Metabolic acidosis. VBGs are a useful screen for pH disturbances. On this VBG, the low pH combined with low bicarbonate concentration is indicative of the presence of a metabolic acidosis. The anion gap is raised.

Note that the machine still ‘thinks’ that it is measuring levels in the arterial blood and the arrows and normal ranges on the printout are indicative of values expected for arterial blood. If you are going to use VBGs, you need to know how these values in venous blood relate to values in the arterial blood (link).

Note that the doctor has circled the lactate concentration on this VBG. Although the level here is very high, and is probably significant, be careful when attaching significance to a marginally elevated lactate level on a VBG. Marginal elevation of the lactate level on a VBG (above the quoted arterial range) is meaningless and may bear no predictable relationship to the arterial level.

ECG/EKG

Afib J3

Afib J4

Atrial flutter with variable conduction. The qrs complexes are narrow and occur at irregular intervals with no underlying pattern. The differential for a truly irregularly irregular rhythm, such as this, includes atrial fibrillation. This, however, is atrial flutter with variable conduction. Note, the characteristic saw tooth appearance of the readout due to the presence of negative (below the isoelectric line; the yellow line) flutter waves (blue). Note that the flutter waves occur at a rate of 300/min (one in every large square). This is typical. However, not all flutter waves are transmitted to the ventricles. This condition is closely related to atrial fibrillation (she may flick in and out of these rhythms). This rhythm disturbance may well be very significant in this case.

Hopefully, you also picked up the right axis deviation. As you can see in the diagram below, the fact that the qrs complexes in lead III are isoelectric means that the cardiac axis must lie in one of the two positions shown in A.  As the qrs complexes are positive in lead aVR, the axis must lie within 90 degrees of this lead meaning that the option illustrated in B is correct. There is marked right axis deviation (normal axis -30 to 90 degrees)The cause of this abnormality is unclear but this is certainly not a normal heart.

axis

Q2. Can you offer a differential diagnosis?

The striking finding, not available to the GP, is the presence of a metabolic acidosis. In a patient with abdominal pain and in atrial fibrillation/flutter, this should raise the possibility of acute embolic mesenteric ischemia (bowel infarction). In fact, the combination of severe abdominal pain with minimal findings on examination, as in our case, is said to be characteristic of this catastrophic condition.

We should also consider the possibility of other intrabdominal catastrophies. Pancreatitis is a well recognised cause of systemic metabolic acidosis and should be excluded.

Metabolic acidosis and tissue infarction

Tissues will switch to anaerobic metabolism generating lactic acid in the presence of ischemia/infarction. If the volume of tissue involved is low, the liver and kidney can work to eliminate the excess lactic acid produced and no systemic acidosis is observed. Therefore, conditions which result in the death of a relatively small volume of tissue, for example, an inferior MI or CVA, although potentially lethal, may not result in a systemic rise in lactate levels or a detectable metabolic acidosis.

Conditions which kill a large volume of tissue will result in a release of lactic acid into the general circulation capable of overwhelming the liver and kidneys ability to eliminate the excess acid giving rise to a systemic acidosis. Classic examples would include, necrosis of the pancreas in acute pancreatitis, necrosis of the liver in, for example, paracetamol (acetminophen) overdose, necrosis of skeletal muscle in a compartment/crush syndrome and, as here, necrosis of bowel in an acute mesenteric ischemia. These pathologies are localised to a particular organ.

In contrast, certain diseases may compromise global tissue oxygen delivery causing widespread ischemia/necrosis in multiple tissues with a resultant lactic acidosis. These include pathologies severely compromising cardiorespiratory function (eg cardiogenic shock, severe respiratory failure) or conditions which result in widespread dysregulation of tissue perfusion (eg disseminated intravascular coagulation (DIC) or septicemia). When you think about it, many of these disorders will be associated with a degree of acute kidney injury further damaging the body’s ability to deal with excess acid.

In general, the presence of a metabolic acidosis is bad news.

Q3. What additional investigations should be carried out?

1) ABG, laboratory electrolytes and an FBC

Bowel infarction CSi

The ABG confirmed the presence of a metabolic acidosis with respiratory compensation. The high lactate level was also confirmed (dumb luck). This lady has lactic acidosis. The laboratory electrolytes confirmed the presence of hyperkalemia. The patient also has an acute kidney injury with elevation of creatinine.

2) Multidetector CT (MDCT) abdomen.

AXR is rarely helpful in the diagnosis of acute mesenteric ischemia. In a suspected case, we carry out an AXR to exclude other causes of the patients symptoms.

MDCT with a dedicated protocol is highly effective in the diagnosis of acute mesenteric ischemia. If IV contrast can be given, the technique can identify the site of embolic occlusion in the affected artery. In this case, after discussion with the radiologists, we avoided IV contrast in view of the acute kidney injury (AKI) evidenced by the raised creatinine.

However, MDCT scan confirmed the presence of air (pneumatosis) in the walls of the bowel and air in the portal vein, both features of bowel infarction. In this case, it was also felt that the left lobe of the liver may also have been involved in an ischemic process.

Dx: acute mesenteric ischemia probably secondary to embolic obstruction of the superior mesenteric artery (SMA).

Amylase

In this case the amylase was elevated. This was a nonspecific finding. There was no evidence of pancreatitis on CT.

Renal US?

Probably not top of the list in this patient’s case. We know the underlying pre-renal cause of her AKI (bowel infarction) and should address same.

Q4. Given the diagnosis established in Q3, what are the therapeutic options?

Therapy of acute mesenteric ischemia must be left to the specialists. Our job, as generalists, is not to miss the diagnosis. However, for exam purposes, we can make a few general points about management.

General management

1) High flow oxygen therapy

2) Aggressive fluid resuscitation with appropriate invasive monitoring on ICU/HDU

3) Heparin anticoagulation

4) Intravenous prophylactic antibiotics (to cover possible bowel perforation)

5) Attention to hyperkalemia

6) Attention to treatment of underlying cause

Direct intervention

This is very specialised area and will depend on multiple factors, most importantly, the surgeon and anaesthetists opinion as to whether the patient can survive intervention. If initial diagnosis is made at angiography, antispasmodics such as papaverine can be infused into the affected artery. Definitive treatment requires surgery. If the patient presents sufficiently early such that bowel infarction has not occurred, it may be possible to perform an embolectomy and salvage the ischemic tissue. If bowel infarction has occurred, as evidenced by findings on CT and evidence of peritonitis on examination, the surgical resection of necrotic bowel will be necessary, if survivable.

Prognosis will depend on several factors. There is evidence that early diagnosis makes a difference. If diagnosed within 24 hours of onset, survival maybe 50% falling to less than 30% if diagnosis is delayed 24 hours.

Q5. What do you make of the original diagnosis of UTI?

Reasonable…. In my experience, bowel infarction is easily missed. The physical signs in the abdomen often do not match the seriousness of the condition. AXR may, as in this case, be normal. The most recent case of acute mesenteric ischemia I have seen was suspected on the basis of a VBG result showing profound metabolic acidosis. The VBG had been carried out simply to obtain electrolyte results in a patient referred with ‘dyspepsia’. The patient was complaining of a considerable amount of pain, however, findings on abdominal examination were minimal. I had planned to request an OGD. I was shocked when the hurriedly arranged CT abdomen confirmed extensive bowel infarction!

Always think of ischaemic bowel when a patient with risk factors for embolic phenomena (eg. atrial fibrillation) presents with acute onset of severe abdominal pain.

but….We are arguably too quick to diagnose UTI in the elderly. The elderly population we deal with nowadays have so much co-morbidity that it is often impossible to be sure, even after fairly extensive investigation, what is causing an acute deterioration in their condition. If the urinalysis ‘comes back positive’ we cling to it, diagnosis made, but this is often not the case. A high proportion of elderly people will have findings on their urinalysis at any point in time irrespective of the presence or absence of urosepsis. A negative urinalysis has value as a test of exclusion, a positive result in the elderly should be greeted with healthy scepticism.

Diagnosis of UTI

On dipstick analysis, the presence of leukocytes and/or nitrites in the urine is taken to be consistent with infection of the urinary tract. Nitrites are produced from nitrates by the types of bacteria typically responsible for urinary tract infections. The presence of nitrites in the urine is, therefore, taken as indicative of the presence of these bacteria in the tract. Leukocytes produce an esterase normally absent from urine. If leukocyte esterase is present in the urine, again, this is taken as a marker of leukocyte infiltration (infection) of the urinary tract. Infection may also be associated with hematuria detected on the dipstick. However, this is a non-specific finding.

False positives and negatives are common on dipstick testing for nitrites and leukocytes and ultimately definitive diagnosis of UTI rests on the demonstration of significant bacterial growth on culture of an MSU in the appropriate clinical scenario. However, this requires time (for bugs to grow) and we often have to act acutely in the absence of this information.

If we get a ‘full house’ 1) typical urinary symptoms (dysuria and/or frequency etc) 2) Urine positive for nitrites 3) Urine positive for leukocytes, then there is a high probability that a UTI is present. This is particularly true if the patient has a documented history of UTIs.

If, as experienced by the GP in this case, we get some combination of these findings, the decision to treat or not to treat is much more difficult.


Subsequent Course

No irsih

In view of her overall clinical state and the extensive nature of the bowel infarction and in conjunction with the surgical consultant on call a decision was made that it would not be possible for her to survive surgical intervention. After discussion with her husband she was commenced on a morphine pump and IV fluids were continued. Treatment of hyperkalemia was withdrawn. She passed away peacefully that night.