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An unusual case Of chest pain

M Rasool Aljabiri
Mrs Smith a 77 - year old Granny
Presented to the (A&E) department with
Acute onset central chest radiating to the back,
not relieved with GTN in A&E

Mild SOB

Palpitations

PMHx: HTN, Hypercholesterolemia and DM type


2. Her medications comprised Simvastatin 40mg,
Atenolol 50mg, Bendrofluazide 25mg, Irbesartan
75mg and Aspirin 75mg.
Chest discomfort had been associated with retching,
but no vomiting.

On examination
she appeared in pain pointing to the middle of her
chest
Her vital signs were;
 PR 71 beats/minute,
 BP 193/83 (no postural drop),
 RR 22 breaths/minute
O2 sats 98% on RA, temperature 37.6oC and
BMs 14.3 mMol/l.
CVS-
Warm peripheries
JVP – N
Apex non displaced
ESM

Respiratory
Chest clear

Abdo
Soft non tender
Nil epigastric tenderness
BS normal
DRE soft formed stool
 Normal Urea and electrolytes

A mild normocytic anaemia with


haemoglobin of 11g/dl was
identified
CRP 16 and WCC 12.5
Clotting Normal
Summary 1
77 Granny
Acute onset Chest pain
SOB
Palpitation
? Retching prior
CXR and ECG
Bloods mildly microcytic anaemia with raised CRP 16
and WCC 12.5
What is the likely diagnosis and what should
her initial management be?

 1) Myocardial ischaemia: aspirin, clexane and clopidogrel whilst
awaiting for a Troponin T.

 2) Pulmonary embolism: clexane at treatment dose whilst awaiting a


CT pulmonary angiogram.

 3) Oesophageal spasm: barium swallow and relief of precipitating


factor.

 4) Dissecting aortic aneurysm: urgent CT chest

 She was initially managed by A&E staff according to the Acute


Coronary Syndrome (ACS) in View of her history of acute CP, HTN,
Hypercholesteraemia ; ASA, Clopidogrel however clexane was
withheld pending a CT as the CXR was suspicious of a dilated
mediastinum
Two hours later she had experienced transient
difficulty in swallowing food. She mentioned to the
Reg that’s what happened when she ate the apple.

Whilst in A&E (waiting for 3 hrs for an acute bed) she


vomited 50ml of fresh blood. (one episode)
She remained stable after the episode of
haematemesis.

The patient was managed conservatively with


intravenous fluids, PPI and NBM. Fluid resuscitation
was commenced

ASA & Clopidogrel were stopped.


A 12 Hour Troponin was negative
No change in her vital signs, no postural drop.
Repeat Urea slightly raised 9
Summary 2
77 Granny
Acute onset Chest pain
Strated on Clexane,ASA,Clopidiogrel
SOB
Dysphagia
Vomiting (haematamesis) X 1, ? Retching prior
CXR and ECG
Stopped clexane and clopidogrel
1)Mallory Weiss tear: urgent gastroscopy with a view to
endoscopic treatment.

2)Oesophageal tear (Boerhaave's syndrome):


gastrograffin swallow and CT chest.

3)Bleed secondary to antiplatelets.

4) Dissecting aortic aneurysm: urgent CT chest.


Now the clever gastroenterologist
comes in,so guess what does he
request?
Suggests an OGD
Within the posterior oesophagus tongue like tissue was seen at 17cm
from the incisors.
As a good registrar , I asked the nurses to call the
consultant to have a look for advice.(on WR)
So the consultant moved the idiot registrar a side.
Of course he didn’t know what was going on either.
Biopsies were taken

A second opinion was sorted within 3 hours of the


endoscopy from a senior consultant
experience played a crucial role here
thought this is oesophageal Apoplexy
The differential diagnosis
Benign ulcer with adherent clot,.
An underlying malignant ulcer,
Transported organised clot within the oesophagus or
oesophageal haematoma/ Apoplexy, secondary to an
underlying tear.
After endoscopy; retrospective hx from the patient,
suggested that 24hr prior to her admission while she
was eating an apple she choked and developed some
difficulty in swallowing that she did not take any
notice off.

Hence a water soluble swallow arranged to


excluded oesophageal perforation.

Then A CT scan was arranged


Water soluble swallow
Spontaneous oesophageal haematomas are a rare consequence of either spontaneous
oesophageal injury or high oesophageal pressure. An underlying disorder of
haemostasis
may be present.[1] A limited number of cases of giant intramural
oesophageal haematoma have previously been described. Bonnette P, Lansac E, Fritsch J: [Intramural
hematoma of the esophagus: a rare diagnosis]. Rev Mal Respir 1999 Dec; 16(6): 1147-50.

The combination of
chest pain,
dysphagia
haematemesis and odynophagia
in association with disorders of haemostasis, fragility of the mucosa, or
trauma of the oesophagus, should evoke the diagnosis.[2-5]
Meulman N, Evans J, Watson A: Spontaneous intramural haematoma of the
oesophagus: a report of three cases and review of the literature. Aust N Z J Surg
1994 Mar; 64(3): 190-3 ,3. Freeman AH, Dickinson RJ: Spontaneous intramural oesophageal haematoma. Clin Radiol 1988 Nov; 39(6): 628-34
Hiller N, Zagal I, Hadas-Halpern I: Spontaneous intramural hematoma of the esophagus. Am J Gastroenterol 1999 Aug; 94(8): 2282-4
Yuen EH, Yang WT, Lam WW: Spontaneous intramural haematoma of the oesophagus: CT andMRI appearances. Australas Radiol May;42(2):139-42 1998

Radiology (thoracic CT scan, barium or water soluble swallow) and endoscopy


enable confirmation of the diagnosis, permitting conservative treatment and simple
spontaneous resolution as in our case (illustration 1). [6-7] the haemorrhage usually
occurs within submucosal/ intramural tissues [6]. Sanaka, Masaki M.D., Ph.D.et al Spontaneous Intramural
Haematoma Localized in the Proximal Esophagus: Truly "Spontaneous"Journal of Clinical Gastroenterology. 27(3) 265-266, October 1998.
Oesophageal haematoma may occur at various sites of the oesophagus.

The mechanism producing the haematoma may determine the site. For
example;

-A haematoma from vomiting would be in the region of the oesophago-


gastric junction.

- A haematoma from a caustic substance might be at points of narrowing.


1. Drugs: coagulation disorders or treatment with various drugs such
as low-dose aspirin.

2. Miscellaneous:
A- Extra luminal causes;
i. Chest trauma
ii. Cardioversion and subsequent anticoagulation.

B- Intra Luminal;
i. Foreign body ingestion
ii. Food-induced injury (as in this case), as a result of abrasive trauma
iii Toxin ingestion
iv. Pill induced oesophageal injury
v. Instrumentation (e.g. endoscopy with variceal sclerotherapy or biopsy,
transoesophageal echocardiogram).
vi. Oesophageal diverticulum, arterio-venous malformation.
vii Aorto-oesophageal fistula.[8] Maher MM, Murphy J, Dervan P: Aorto-oesophageal fistula presenting as a
submucosal oesophageal haematoma. Br J Radiol 1998 Sep; 71(849): 972-4
viii.Coughing, retching and prolonged vomiting

C- Oesophageal Barotraumas.
Stages of haematoma [9]

I)Haematoma without surrounding tissue oedema, these patients are


normally asymptomatic.

II)Haematoma with surrounding tissue oedema, e.g. after an oesophageal


biopsy.

III) Haematoma with oedema plus compression of the oesophageal lumen -


oedema and separation of the surface mucosal layer partially
obliterates the lumen.

IV)Complete obliteration of the lumen with haematoma, oedema and


organized clot formation – resulting in absolute dysphagia.
Endoscopic appearance of the oesophagus at 17cm from the incisors eight weeks post
discharge: complete mucosal healing with no evidence of tumour.
•The diagnosis of Oesophageal Apoplexy / Haemorrhage is rare; therefore a clear
management approach has not yet been established.

•For spontaneous intramural haematoma, conservative therapy leads to an excellent


prognosis.

•Oesophageal haematomas usually resolve within 10-14 days.[1]

•Once the diagnosis is suspected the patient should be made NBM and the upper GI
surgeons informed.

•Acid suppression should be considered to reduce the risk of oesophageal ulceration and
correction of any coagulation abnormalities is indicated.

•Investigations, as discussed above, should be undertaken to confirm the diagnosis.

•Once the patient is stabilised (which may take 4-6 days) a soft diet may be started.

•Endoscopic sclerotherapy, used previously when extensive oesophageal haematoma was


present, has the associated risk of rupture of the intramural haematoma.[9-10] and thus
is not routinely indicated.

•Massive ongoing haematemesis, reported in an earlier literature review as


occurring in 19% of 31 patients presenting with oesophageal haematoma, is the only
indication for surgery. [10]
References:

1. Bonnette P, Lansac E, Fritsch J: [Intramural hematoma of the esophagus: a rare


diagnosis]. Rev Mal Respir 1999 Dec; 16(6): 1147-50.
2. Meulman N, Evans J, Watson A: Spontaneous intramural haematoma of the
oesophagus: a report of three cases and review of the literature. Aust N Z J Surg
1994 Mar; 64(3): 190-3
3. Freeman AH, Dickinson RJ: Spontaneous intramural oesophageal haematoma.
Clin Radiol 1988 Nov; 39(6): 628-34
4. Hiller N, Zagal I, Hadas-Halpern I: Spontaneous intramural hematoma of the
esophagus. Am J Gastroenterol 1999 Aug; 94(8): 2282-4
5. Yuen EH, Yang WT, Lam WW: Spontaneous intramural haematoma of the
oesophagus: CT andMRI appearances. Australas Radiol May;42(2):139-42 1998
6. Sanaka, Masaki M.D., Ph.D.et al Spontaneous Intramural Haematoma Localized
in the Proximal Esophagus: Truly "Spontaneous"Journal of Clinical
Gastroenterology. 27(3) 265-266, October 1998.
7. Cullen SN,Chapman RW: Dissecting intramural haematoma of the oesophagus
exacerbated by heparin therapy. QJM 1999 Feb; 92(2): 123-4.
8. Maher MM, Murphy J, Dervan P: Aorto-oesophageal fistula presenting as a
submucosal oesophageal haematoma. Br J Radiol 1998 Sep; 71(849): 972-4.
9. Ouatu-Lascar R, Bharadhwaj G, Triadafilopoulos G.Endoscopic appearance of
esophageal World J Gastroenterol, 2000;6(2):307-309
10. Skillington PD, Matar KS, Gardner MA: Intramural haematoma of the
oesophagus complicated by perforation. Aust N Z J Surg 1989 May; 59(5): 430-2

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