Bradycardia or paradoxical bradycardia can be a sign in ruptured ectopic pregnancy

Picture showing a Tubal Pregnancy with a human embryo in 7th week pregnancy

Courtesy of Ed Uthman, MD (released into public domain)

We often think that in cases of intra-abdominal hemorrhage, tachycardia is most often the first physical manifestation. We recently saw a case of ruptured ectopic pregnancy that presented with bradycardia. Actually, a number of literature has shown that bradycardia is a well-established phenomenon noted in cases of hemoperitoneum, including ruptured ectopic pregnancy.

Similarly, in cases of traumatic hemorrhage, about a third of these patients can present with bradycardia even in the face of acute reduction in blood volume.

Although the exact mechanism for this phenomenon is not known, the hypothesized pathophysiology behind this relative or paradoxic bradycardia is vagal stimulation, either from the mechanoreceptors in the left ventricle or triggered by blood in the peritoneum.

The emergency physician should also be aware that because of the possibility of heterotopic pregnancy, the presence of an intrauterine pregnancy cannot still exclude the possibility of a concurrent ectopic pregnancy especially if the clinical signs are suggestive.

Also, a pelvic ultrasonographic examination demonstrating an empty uterus is sufficient to diagnose ectopic pregnancy if the quantitative Beta-hCG level is high enough.

Click here to download a short case report article illustrating this phenomenon.

References:
1. Somers MP, Spears M, Maynard AS, Syverud SA. Ruptured heterotopic pregnancy presenting with relative bradycardia in a woman not receiving reproductive assistance. Ann Emerg Med. 2004 Mar;43(3):382-5.

2. Thomas I, Dixon J. Bradycardia in acute haemorrhage. BMJ. 2004 Feb 21;328(7437):451-3. Click here to access free.

New 2012 Berlin Definition for ARDS

The new 2012 definition for Acute Respiratory Distress Syndrome (ARDS) (published in JAMA June 2012)

According to the previous definition published in 1994 by the American-European Consensus Conference (AECC), ARDS must have the following 4 criteria:

• the onset must be acute
• there must be hypoxemia with PaO2/FIO2 ratio ≤ 200
• there must be bilateral infiltrates on CXR
• these findings cannot be attributed to other causes

A separate category for acute lung injury (ALI) is defined with PaO2/FIO2 ≤ 300

However, a number of problems are found with the 1994 definition, including:

• term 'acute' was not defined (i.e., how "acute" is acute)
• the category of ratio PaO2/FIO2 between 201-300 is confusing (PaO2/FIO2 ≤ 300 is ALI, PaO2/FIO2  ≤  200 is ARDS, PaO2/FIO2 between 201 - 300 ?ALI/ARDS)
• CXR interpretation has poor inter-observer reliability

With this, the new Berlin 2012 definition of ARDS is published with the following changes:

1. the category of acute lung injury (ALI) with PaO2/FIO2 ≤ 300 is REMOVED
2. instead, ARDS is now divided into three categories based on severity of hypoxemia
1. PaO2/FIO2 between 200–300 is defined as mild
2. PaO2/FIO2 between 101 - 199 is defined as moderate
3. PaO2/FIO2 of less than 100 is defined as severe
3. The term 'acute' now has a specified time frame of symptoms developing within ONE week of a known clinical insult
4. Other changes:
1. the CXR criteria is now more defined with the added phrase "bilateral opacities - not fully explained by effusions, lobar/lung collapse, or nodules"
2. PCWP reading is no longer required as part of the diagnosis as this is increasingly not used. Instead, this new definition requires that the respiratory failure cannot be explained fully by cardiac failure or volume overload.

Editorial comment in JAMA June 2012 points out that this new definition only improves its predictive value of mortality slightly; however, the clarity of the criteria is significantly improved.

Ref:The ARDS Definition Task Force. Acute respiratory distress syndrome: The Berlin definition. JAMA 2012 Jun 20; 307:2526
Abstract: http://jama.jamanetwork.com/article.aspx?articleid=1160659

A case of recurrent abdominal distension

A 50-year old man with recurrent history of unable to pass stools for 3 days’ duration with abdominal distension. Otherwise he appears comfortable. On examination, abdomen is distended, but soft and non-tender on palpation. Bowel sounds were diminished. He had multiple admissions for similar complaints for the last two years. The abdominal x-ray for the current admission is as below:

And the abdominal x-ray taken 9 months ago when he was admitted similarly is as below:

Further history revealed that when he presented for the first time, the surgical team performed an exploratory laparatomy and found no abnormality. He has history of schizophrenia and is on antipsychotics. 

What diagnosis should you consider in this case?


Ans: recurrent colonic pseudo-obstruction also known as Ogilvie Syndrome.

Pathophysiology:

1. When Ogilvie first described these cases, he hypothesized that the etiology was due to sympathetic deprivation to the colon, leading to unopposed parasympathetic tone, resulting in regional contraction, and thus functional obstruction.

2. However, the current understanding is, unlike the hypothesis Ogilvie proposed, is because of parasympathetic suppression (in this case, sacral parasympathetic outflow), or excessive sympathetic stimulation (Maloney & Vargas, 2005)

RECALL that:
the parasympathetic nervous system increases gut motility and
the sympathetic nervous system decreases gut motility

Thus, in the presence of disruption of the parasympathetic stimulation, results in reduced gut motility or adynamic of distal gut segment, resulting in functional dilatation. This hypothesis is supported by the use of neostigmine in the treatment of this condition.

3. Neostigmine is an acetycholinesterase inhibitor (Ponec et al, 1999).
Acetycholinesterase results in the breakdown of acetylcholine into acetate and choline.
Thus, neostigmine, by inhibiting the action of this acetylcholinesterase, inhibits the breakdown of acetylcholine (by the same token, neostigmine can be used to treat myastenia gravis by increasing the concentration of acetycholine)

4. The cecum is the usual site of the largest dilatation in Ogilvie syndrome and, thus, is more prone to the risk of perforation. This is because cecum has a large diameter. Laplace law states that the intraluminal pressure needed to stretch the wall of a hollow tube is inversely proportional to its diameter.  Thus, because of its large diameter, it is easier to overcome the wall tension of cecum with a small amount of pressure than with other parts of the gut (Click here to access the article in emedicine)

5. Of course, this syndrome has to be a diagnosis of exclusion. Mechanical obstruction has to be ruled out. In this patient, exploratory laparatomy was first performed and the gut was found to be normal.


6. The patient is on anti-psychotic drugs. Many of these anti-psychotics such as phenothiazines have anticholinergic properties; thus aggravate this patient's condition.

Click here for a chapter on Ogilvie Syndrome

One should also differentiate toxic megacolon from Ogilvie syndrome. However, the clinical features in toxic megacolon are quite different from this syndrome. Patient with toxic megacolon is rather sick looking. Jalan criteria for toxic megacolon are:

• Radiographic evidence of colonic dilatation - The classic finding is more than 6cm in the transverse colon PLUS
• Any 3 out of 4 of the following
• Fever (>38.6C)
• Tachycardia (>120/min)
• Leukocytosis (>10.5 x 103/µL) or 
• anemia  PLUS
• Any 1 of the following - Dehydration, altered mental status, electrolyte abnormality, or hypotension
  

(Jalan KN, Sircus W, Card WI, Falconer CW, Bruce CB, Crean GP, McManus JP, Small WP, Smith AN. An experience of ulcerative colitis. I. Toxic dilation in 55 cases. Gastroenterology. 1969 Jul;57(1):68-82.)




References:
1. Maloney N, Vargas HD. Acute intestinal pseudo-obstruction (Ogilvie's syndrome). Clin Colon Rectal Surg. 2005 May;18(2):96-101. Click here for free full text in pdf

2. Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudo-obstruction. N Engl J Med. 1999 Jul 15;341(3):137-41. Click here for free full text.