Monday, 4 January 2010

Look at the patient

Dear Bloggers

Although technology has taken medicine into a new age, we should not leave the fundamental skills of doctoring behind.

The following case is a vignette and has been anonymised to safe-guard patient confidentiality.

An elderly lady of 86 years of age had been admitted to a hospital with severe dehydration, vomiting and abdominal distension and she was tentatively diagnosed with paralytic ileus. The patient was treated with intravenous fluid and kept nil by mouth with nasogastric tube suctioning whilst undergoing investigation for the cause.

The patient had a urinary catheter placed to measure urine output and post-renal obstruction had been excluded by a normal appearance of kidneys, ureters and bladder on ultrasound scan. High doses of furosemide were also used at the same time as the intravenous fluid with the aim to 'kick start' her ailing kidneys and to avoid heart failure.

A plain CT of the abdomen had shown distal loading of the large colon with faeces and dilated small loops of bowel.

Initial blood gas on the admission revealed a severe metabolic acidosis.

Several days into the admission, the patient started to produce bloody coloured fluid from the NG tube, and upper GI bleeding was strongly suspected. Intravenous proton pump inhibitor therapy was commenced in addition to continuing fluid resuscitation whilst awaiting gastroscopy.

However, the patient's heart rate was then seen to slow on the monitor to 40/min and last the recorded blood pressure was 160/80mmHg. Initially, the physicians were looking at the monitor abnormality, but when the patient was assessed, she was found to be completely unresponsive and there was no respiratory effort. After pulse check, there was found to be no cardiac output. Pulseless Electrical Activity (PEA) was immediately considered and CPR was commenced.

In addition to the blood in the NG tube, the diaper also contained fresh pungent malaena.

This patient's circulation was initially restored with crystalloid fluids (several litres) and later with red cell transfusions, in addition to using atropine, adrenaline and high dose dobutamine support. However, the initial haemorrhagic shock and use of vasoconstrictors resulted in cardiac ischaemia. Moreover, it was unclear how long the patient had been in cardiac arrest prior to starting CPR and despite restoration of her circulation, there was no improvement in cerebral function with GCS of 3/15. Despite the resuscitation, the patient appeared inotrope-dependent, a commonly seen sequal to cardiac arrest. Unfortunately, the patient reverted to PEA and despite further attempts at CPR, she could not be revived.

An autopsy was performed which revealed an acute duodenal ulcer and distal ischaemic colitis.

The Learning Points from This Case Vignette

If there is a monitoring abnormality, look at the patient and recheck the vital signs, manually if need be, and repeat the physical examination. You should seek out the cause.

Remember to Check the Airway, Breathing and Circulation in unresponsive patients.
Focusing only on the monitor can distract you away from the patient - remember that both are important.

A bleeding patient needs rapid assessment and restoration of circulation with fluids and blood +/- clotting factors (if required).

Circulation is difficult to assess and this can be improved by placing a central venous line to monitor the central venous pressure.

Urine output needs to be measured hourly to ensure that there is no deterioration. Often, the urine output drops consistently in shocked patients before they develop cardiac arrest -- this depends on the velocity of bleeding -- it can be an early warning sign of problems to come.

Low pulse rate needs assessing just the same as high pulse rate -- this patient should have developed a tachycardia but instead had bradycardia which might reflect a severely ischaemic heart e.g. from severe bleeding on a background of coronary heart disease.

In acutely unstable GI bleeders, the endoscopy equipment can be brought to the bedside and therapeutic intervention can be done there and then. It may not be safe or practical to wait and despite the best attempts to stabilise the patient so as to get them to the endoscopy suite, it is sometimes not possible. Doing intervention at the bedside is sometimes the only viable way.

Unstable GI bleeders need to be in a monitored bed e.g. a high dependency unit, acute bleeder bed, or an ICU. They should not be managed on a general ward if they are unstable.

Group and Save blood for all bleeding patients. Those with significant losses should be cross matched and transfused rapidly. Don't rely on the haemoglobin level in acute GI bleeding as it can be falsely normal. If there is no time for the cross match then give Group O blood (universal donor) until the cross matched blood is available. Don't wait for your patient to bleed out.

Inform the surgeons in the case of a patient who is admitted with upper GI bleeding. Doctors may sometimes become over confident that 'it's just another GI bleeder' until the disaster of when the patient bleeds out. If the upper GI bleed cannot be resolved through conservative methods e.g. clipping, cautery, hypertonic saline-adrenaline, transfusions etc, the patient should be considered for surgical intervention. However, if the surgeons hear about the patient for the first time as 2 litres of malaena hit the floor, they will not be very pleased with you for telling them at the last minute. Remember, it is better to operate on a patient who is stable than on one who is unstable and which situation could have been avoided if preparations had been taken sooner. Have a low threshold for getting a surgical opinion early.

Do not be blase' about GI bleeding. It is serious and as the above vignette case demonstrates, it can lead to serious consequences. In this case, the upper GI bleeding led to unexpected and profound haemorrhagic shock and then PEA.

When you have a monitor showing unusual readings, look at it in combination with the patient. The monitor is a guide and not an absolute. Unless the patient is linked to direct arterial pressure monitoring, or transoesophageal cardiac output monitoring, it may not be possible to know that PEA has occurred. Relying on an ECG rhythm strip can be misleading especially if there is implantation of a pacemaker. Look at the patient! Check the carotid pulse. Sometimes the most simplest of things can be the most significant and helpful.

This brings me back to a previous issue of an Early Warning System -- a UK idea of several years standing, that scores patients according to their vital signs. If there is a deterioration from the normal variability, then the score rises and once a threshold is met, the doctor is called for the patient to be reassessed. Many UK hospitals utilise this system for spotting the 'deteriorating patient' with the aim to avoid problems.

The drop in pulse and an unresponsive patient would have resulted in an EWS score of 5 (>4 = call doctor as soon as possible). The low amount of urine in the catheter bag is another tell tale sign of problems. Such a low output without evidence of urinary tract obstruction makes one consider either pre-renal or intrinsic renal failure. In the event of bleeding, the former is a more likely cause.

When we look at the BUN and creatinine of a patient, don't just think dehydration if the ration of BUN-to-Creat is increased. Also think Bleeding specially if the ratio >20:1 ! This means performing a rectal examination looking for blood, passing an NG tube to check for upper GI haemorrhage, and serial haemoglobin measurements (plus renal function tests too) in addition to repeated physical examinations of the patient to look for signs of ensuing hypoperfusion e.g. cold extremities, confusion, decreased urine output etc....

Providing intravenous fluids AND diuretics to 'kick start' the kidneys is NOT the standard way to treat a hypovolaemic patient. Remember, when a patient is hypovolaemic, there is increased output of vasopressin and angiotensin II to cause the reabsorption of H2O and Na+, to try and stabilise the blood pressure and hence, renal blood flow. It is therefore no surprise that the urine is decreased and concentrated in hypovolaemia. The important thing is to replace volume to improve perfusion but NOT using diuretics as this makes matters worse by decreasing the intravascular volume yet further.

Moreover, patients can develop acute tubular necrosis which has an initial oliguric phase followed by a diuretic phase. This can be avoided if there is adequate fluid resuscitation performed early. To understand fluid status more accurately, a CV line should be placed. There is no additional benefit placing a Swan-Gantz catheter. Some physicians rely whole heartedly on the IVC compliance measurement (as assessed by echocardiogram) to make decisions, with them sometimes ignoring all other evidence of hypovolaemia when an IVC compliance appears normal, at the potential detriment to the patient. Remember, no one physical sign and/or test is always going to give the right answer, but usually a combination of signs and/or tests does. Also, the result of an echocardiogram is only as good as the practitioner performing it.

Please try and look at the overall picture of the patient and remember that it is better to give generous fluids rather than judicious fluids and catecholamines with the latter causing the potential risk of arterial ischaemia and organ failure if used inappropriately. Consider heart failure as a potential outcome of too much fluid but do not let that stop you giving adequate fluid resuscitation. Boluses of fluid to maintain circulation and re-examining for heart failure is one way to try and gauge how much fluid to infuse into the patient.

If after fluid resuscitation is performed and CVP is adequate e.g. 12cm H20, and BP still remains low, then giving catecholamines is justifiable e.g. septic shock, cardiogenic shock, adrenal failure etc, but certainly NOT diuretics as an initial therapy to try and 'kick start' kidneys or to try and avoid possible heart failure.

In summary, let's get back to basics and review the patient's status through physical examination rather than just looking at numbers and blips on a screen. The 'red flag' signs of GI bleeding e.g. haematemesis, malaena, hypotension and low urine output, are serious and require immediate assessment and intervention. No inpatient being actively treated should succumb to GI bleeding without having first, established a cause, and secondly, having attempted to abrogate the problem. Remember the H's and T's of the reversible causes of cardiac arrest of which Hypovolaemia (including haemorrhage) is one.

I hope this is food for thought. Have a good week.

1 comment:

Blog Administrator said...

International Consensus Recommendations on the Management of
Patients With Nonvariceal Upper Gastrointestinal Bleeding

Alan N. Barkun, MD, MSc (Clinical Epidemiology); Marc Bardou, MD, PhD; Ernst J. Kuipers, MD; Joseph Sung, MD; Richard H. Hunt, MD;
Myriam Martel, BSc; and Paul Sinclair, MSc, for the International Consensus Upper Gastrointestinal Bleeding Conference Group*

Description: A multidisciplinary group of 34 experts from 15 countries developed this update and expansion of the recommendations
on the management of acute nonvariceal upper gastrointestinal
bleeding (UGIB) from 2003.

Methods: The Appraisal of Guidelines for Research and Evaluation (AGREE) process and independent ethics protocols were used. Sources of data included original and published systematic reviews; randomized, controlled trials; and abstracts up to October 2008.

Quality of evidence and strength of recommendations have been rated by using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) criteria.

Recommendations: Recommendations emphasize early risk stratification,
by using validated prognostic scales, and early endoscopy (within 24 hours). Endoscopic hemostasis remains indicated for high-risk lesions, whereas data support attempts to dislodge clots with hemostatic, pharmacologic, or combination treatment of the underlying stigmata. Clips or thermocoagulation, alone or with epinephrine injection, are effective methods; epinephrine injection alone is not recommended. Second-look endoscopy may be useful
in selected high-risk patients but is not routinely recommended.
Preendoscopy proton-pump inhibitor (PPI) therapy may downstage the lesion; intravenous high-dose PPI therapy after successful endoscopic hemostasis decreases both rebleeding and mortality in patients with high-risk stigmata. Although selected patients can be
discharged promptly after endoscopy, high-risk patients should be hospitalized for at least 72 hours after endoscopic hemostasis. For patients with UGIB who require a nonsteroidal anti-inflammatory drug, a PPI with a cyclooxygenase-2 inhibitor is preferred to reduce rebleeding. Patients with UGIB who require secondary cardiovascular prophylaxis should start receiving acetylsalicylic acid (ASA) again
as soon as cardiovascular risks outweigh gastrointestinal risks (usually within 7 days); ASA plus PPI therapy is preferred over clopidogrel alone to reduce rebleeding.

Ann Intern Med. 2010;152:101-113.