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SELF ASSESSMENT QUESTIONS
Recurrent abdominal pain—the forgotten cause
P M S Evans, A Williams, A H El-Shaboury
A 23 year old man presented to the casualtydepartment with right
periorbital oedema. Adiagnosis of urticaria was made,
antihistamineswere prescribed, and he was discharged home.Within 24
hours he returned complaining ofincreased facial swelling and
dysphagia, and amedical opinion was sought. He denied recentfacial
trauma, or insect stings. Further inquiryrevealed that he had
suVered a similar episodenine months earlier which had involved
swell-ing of his hands and feet. These areas were notitchy or red.
His past history included recur-rent bouts of abdominal pain
associated withdistension and vomiting requiring numeroushospital
admissions under the care of diVerentconsultants over the previous
14 years. A diag-nosis of abdominal migraine was
frequentlyrecorded. There were no obvious precipitatingfactors and
the bouts resolved spontaneouslyover a period of a few days.
Detailed familyhistory uncovered several members with simi-lar
symptoms and an inheritance pattern alongthe maternal line.
Examination revealed a slimbuilt, normotensive 23 year old man with
bilat-eral periorbital, perioral, and pharyngealoedema. He was
comfortable at rest with nodrooling, dyspnoea, or wheeze (fig 1).
Routineinvestigations showed a normal full bloodcount, urea and
electrolytes, liver functiontests, and chest x ray film. The
suspected diag-nosis of C1 esterase inhibitor (C1 INH)deficiency
was confirmed with low C1 INHand C4 concentrations at 0.08 g/l
(normal0.15–0.35) and
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A rare coincidence and recurrent urinary tractinfections
D Debnath, D G Richards
A 68 year old woman was referred for recurrentepisodes of
urinary tract infection and weightloss of four months’ duration.
She gave ahistory of intermittent brownish dischargefrom her
urethra for the same duration but wasotherwise asymptomatic. There
was no signifi-cant past medical history. Laboratory evalua-tion
revealed a haemoglobin level of 100 g/l,leucocyte count of 11.0 ×
109/l, and a positiveurine culture (Escherichia coli). A rigid
cystos-copy was performed which readily confirmedthe diagnosis. A
biopsy specimen, which wastaken during cystoscopy, showed
transitionalcell carcinoma.
Computed tomography of abdomen andpelvis (fig 1) was arranged.
There was no nodalspread or liver metastasis. She
subsequentlyunderwent laparotomy that revealed the fistu-lous
communication between sigmoid colonand roof of the bladder. A
defunctioning colos-tomy was performed. She was recalled after
sixweeks for a second operation that entailed atotal cystectomy
(along with ileal conduitformation) and low anterior resection with
clo-sure of the rectal stump and left iliac fossacolostomy. Her
postoperative recovery wasuneventful.
The whole specimen was sent to the patholo-gist for further
evaluation (fig 2 is the micro-photograph of relevant section of
the histology).
Questions(1) What is the initial diagnosis?(2) What and how
common are the histologi-
cal findings?(3) What is the prognosis?
Answers on p 129.
Figure 1 Computed tomography of abdomen and pelvis.
Figure 2 Histology (haematoxylin and eosin; original
magnification × 100).
122 Self assessment questions
West CumberlandHospital, Whitehaven,CumbriaD DebnathD G
Richards
Correspondence to:Mr D Debnath, c/o NortonHouse, Grantham
andDistrict Hospital, 101Manthorpe Road, Grantham,Lincolnshire NG31
8DG,[email protected]
Submitted 8 December 1999Accepted 22 December 1999
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Obtunded sensorium in a trauma patient
A Mazumdar, S Kumar, S P Balasubramanian, A K Sharma
A 36 year old man, a victim of road traYc acci-dent, with head
injury and epistaxis, was takento a district hospital. He was
intubated with anorotracheal tube and his scalp injury wasdressed,
and he was referred to this tertiary careinstitute accompanied by
his relatives. Threehours after the injury, when he was brought
tothe emergency room, he was noted to have inter-costal recession
while breathing, a systolic bloodpressure of 95 mm Hg, and Glasgow
coma score(GCS) was 2/10. Air entry on both sides of thechest was
minimal and equally diminished onboth sides, the percussion note on
either sidewas not dull, and the neck veins were empty.Flow from
the endotracheal tube was hardlyaudible. An endotracheal suction
catheter wasinserted but it could not be pushed beyond 20cm.
Arterial blood gases were sampled whiletrying hard to ventilate
with an Ambu bag andwere: oxygen tension 10.4 kPa, carbon
dioxidetension 6.9 kPa, and pH 7.26. As per referralnote, his
systolic blood pressure at the time ofreferral was 110 mm Hg and
GCS 5/10. Therewas no apparent external loss of blood. (Moni-toring
by pulse oximetry was not possiblebecause no pulse oximeter was
available.)
Questions(1) What is the most likely cause of deteriora-
tion of GCS in this case?(2) What should be the next step?(3)
What is the most probable cause of hypo-
tension in this case?(4) What is the finding shown in fig 1?(5)
What is the most likely explanation for the
development of blockage of this endotra-cheal tube?
Acute appendicitis: an unusual cause
S K Clark, T Qureshi, M Sen
A 52 year old woman presented with a two dayhistory of worsening
central abdominal pain,with nausea, and vomiting. Over the
previousmonth she had been treated for a flare up ofrheumatoid
arthritis. Her only medication wasmethotrexate 10 mg/week and
buprenorphine200 µg three times a day. On examination shelooked
unwell and had a pyrexia of 37.4°C.Her pulse was 110 beats/min and
her bloodpressure was 110/54 mm Hg. Her abdomenwas distended and
she had generalised periton-ism; bowel sounds were absent. She had
a mildleucocytosis of 11.2 × 109/l but her full bloodcount and
serum electrolytes were otherwisenormal. Plain abdominal
radiography revealedmultiple central loops of small bowel whichwere
not dilated.
At laparotomy there was free pus in the pel-vis, and a pelvic
appendix was inflamed andperforated distally; the only other
abnormali-ties were a 10 cm nodular cyst of the right ovaryand
inflammation of the omentum. Appendi-cectomy, right
salpingo-oophorectomy, andomentectomy were performed. These
organswere non-adherent and were therefore re-moved separately.
Questions(1) Describe the histological features
(see p 131).(2) What further treatment is indicated?
Answers on p 130.
Figure 1 Blocked endotracheal tube extubated frompatient with
deterioration in sensorium.
Department ofSurgery,Crawley Hospital,Crawley,West Sussex, UKS K
ClarkT QureshiM Sen
Correspondence to:Miss S K Clark,25 Kelso Place,London W8 5QG,
UK
Submitted 8 July 1999Accepted 22 December 1999
Answers on p 130.
Self assessment questions 123
Department ofSurgery, PostGraduate Institute ofMedical Education
&Research, Chandigarh,IndiaA MazumdarS KumarS P
BalasubramanianA K Sharma
Correspondence to:Mr Ajay Sharma, RenalTransplant Unit, Link
9C,Royal Liverpool UniversityHospitals, Prescot Street,Liverpool L7
8XP, UK
Submitted 14 June 1999Accepted 22 December 1999
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Is spiral computed tomography the imagingmodality of choice for
renal colic?
N Sarath Krishna, L Morrison, C Campbell
A 59 year old women was admitted with left loinpain of three
days’ duration. There was noradiation of pain to her groin. She had
no dysu-ria, urinary frequency, or vaginal discharge andwas
apyrexial. On examination she had no lointenderness. She was
treated with analgesics,which relieved her pain. Her urine analysis
waspositive for blood. A midstream specimen ofurine showed no
growth of organisms. Fullblood count, electrolytes, urea, and
creatininewere all within normal limits. Intravenous urog-raphy was
performed which revealed no obviouscalculus in the line of the
urinary tract and anormal right kidney. A delayed dense nephro-gram
was seen on the left side. There was nocontrast excretion into the
left ureter. Subse-quently spiral computed tomography of theabdomen
was performed to exclude a calculusas the cause of the obstruction
(see fig 1).
Questions(1) What is the diagnosis, and what is spiral
computed tomography?
(2) What are the findings on the spiral com-puted tomogram?
(3) What are the advantages of spiral com-puted tomography in
evaluating a case ofrenal colic?
A young woman with intractable diarrhoea
A S Kashyap, R Varadarajulu, S Kashyap
A 28 year old saleswoman reported loosemotions of three years’
duration. She wassymptomatic with recurrent copious wateryloose
motions five to six times a day, which hadprogressively worsened.
Symptomatic treat-ment with antimotility agents had providedpoor
relief.
Moderate hypertension had been diagnosedseven years before,
which was controlled withenalapril 5 mg/day. Over a period of four
yearsher blood pressure settled to normal levels.Enalapril was
discontinued three years ago andher blood pressure remained normal.
Herfather had died suddenly of hypertension and“abdominal
tumour”.
On clinical examination her blood pressurewas 130/76 mm Hg with
no postural fall. Therest of the general and systemic
examinationwas normal. Her packed cell volume, completeblood
counts, peripheral blood smear, serumpotassium, sodium, calcium,
phosphate, albu-min, glucose, serum creatinine, thyroid
profile,stool microscopy and culture, fecal fat excre-tion,
D-xylose absorption test, upper gastro-intestinal endoscopy,
colonoscopy, small intes-tinal biopsy, small bowel barium
followthrough, abdominal and chest radiographswere normal. HIV
antibodies were negative byenzyme linked immunosorbent assay.
The
serum and urine drug, toxicology, and laxativescreen were
negative. The serum concen-trations of serotonin, gastrin,
somatostatin,vasoactive intestinal peptide, and calcitoninwere
normal. Concentrations of urinary5-hydroxyindole acetic acid and
plasma nore-pinephrine and epinephrine were normal. Theplasma
dopamine concentration was 0.94ng/ml (normal
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acid was 13 mg/day (normal
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A small axillary nodule—a therapeutic dilemma?
A Mazumdar, R K Vasishta, S M Bose
A 75 year, postmenopausal women presentedwith a lump in the left
axilla associated withoccasional pain for six months. There was
nohistory suggestive of an increase in size, anawareness of a lump
in either breast or theopposite axilla, or discharge from the
nipple.Past medical history was not contributory asthere was no
family history of breast cancer.Examination showed a firm, mobile
lump inthe centre of left axilla (1× 1 cm), subcutaneousin
location. No other lump could be detected inthe axilla or either of
the breasts.
The patient had been seen earlier by ageneral practitioner who
considered the lumpof benign pathology. Fine needle
aspirationcytology (FNAC) carried out in our hospitalrevealed
features suggestive of metastatic carci-noma. Excision biopsy
showed it to be an infil-trating duct carcinoma. Chest
radiography,ultrasonography of the abdomen, and
bilateralmammography were normal.
The patient underwent total mastectomyand axillary clearance
with excision of the axil-lary scar. Histopathology revealed no
primaryfocus in the entire breast or lymph nodes in theaxilla.
Sections from the excised scar tissueshowed a very small focus of
malignancy (fig1). The postoperative period was uneventful.An
oestrogen receptor study was positive. The
patient is followed up regularly and takingtamoxifen 20 mg once
a day.
Questions(1) What is the significance of an axillary
nodule in an elderly patient?(2) What should be the diagnostic
modality
in a case of axillary nodule?(3) What is the treatment modality
in a case
of axillary nodule with occult metastasis?(4) What are the
various histopathological
considerations in such a case?
A farmer with artificial valve endocarditis
H Alsoub, S S El-Shafie
A 29 year old Yemeni man, a farmer, with StVincent aortic and
mitral prosthesis replaced inApril 1996, was admitted to hospital
in Febru-ary 1997 with a nine month history ofintermittent fever,
general weakness, and lossof appetite. Three months before
admission hedeveloped right sided hemiparesis for which hewas
admitted to another hospital. No details ofthat admission could be
obtained, however hehad significant improvement in his
weakness.Physical examination on admission revealed:temperature
39oC, blood pressure 120/60 mmHg, pulse 104 beats/min, an early
diastolicmurmur at the left sternal border, and mildright facial,
right upper, and lower limbweakness. Laboratory investigations
revealedthe following: haemoglobin 99 g/l, white cellcount 4.3 ×
109/l, platelet count 288 × 109/l,erythrocyte sedimentation rate
(ESR) 33 mmin the first hour, and brucella agglutination testand
mercaptoethanol test were positive to titres
of 1: 5120 and 1:2560 respectively. Liver andrenal function
tests were normal. A trans-oesophageal echocardiogram revealed
small
Answers on p 135.
Figure 1 Microphotograph showing nest of tumour cellsbeneath the
skin in the subcutaneous plane.
Hamad MedicalCorporation, PO Box3050, Doha, QatarH AlsoubS S
El-Shafie
Correspondence to:Dr Alsoub
Submitted 18 February 1998Accepted 7 December 1999
Answers on p 136.
Figure 1 Two dimensional echocardiogram, parasternallong axis
view showing prosthetic aortic and mitral valves.Note the
separation between the aortic wall and theprosthesis ring (arrow);
LV = left ventricle; RV = rightventricle; LA = left atrium.
126 Self assessment questions
Post GraduateInstitute of MedicalEducation andResearch,
Chandigarh,India: Department ofSurgeryA Mazumdar
Department ofPathologyR K Vasishta
Surgery Unit II andEmergency ServicesS M Bose
Correspondence to:Professor S M Bose, H No75, Sector 24,
Chandigarh,160023 Indiasmbose>[email protected]
[email protected]
Submitted 21 September1999Accepted 20 December 1999
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vegetation at the aortic prosthesis with moder-ate paravalvular
leak, the mitral prosthesis wasnormal (fig 1). Six blood cultures
grew Brucellamelitensis. He was treated with oral doxycycline100 mg
twice daily, rifampin 450 mg twicedaily, and intravenous
co-trimoxazole 960 mgthree times daily. Four days later he was
takenfor operation, two ring abscesses were found,they were
drained, and the infected valve wasreplaced by a new one. Culture
of speci-menstaken during surgery yielded B melitensis.He had an
uneventful postoperative course and
was discharged two weeks later on oral doxycy-cline, rifampin,
and co-trimoxazole, which hetook for a total of 20 weeks.
Questions(1) What are the most common organisms
causing artificial valve endocarditis? Whatare other less common
organisms shouldbe considered?
(2) How should the diagnosis be established?(3) What would be
the best therapeutic
approach?
Loss of weight in a female heavy smoker withdiVuse interstitial
pulmonary fibrosis
A Al-Adsani, M H Dahniya, N Al-Adsani
A 75 year old hypertensive woman was admit-ted with a two month
history of fever andcough with scanty sputum, loss of appetite
andweight, and progressive exertional dyspnoea.She had habitually
smoked 20–40 cigarettes aday since the age of 19 years. Her
activities hadbecome limited recently by dyspnoea and backpain.
There was no history of exposure totuberculosis. Chest radiography,
done twoyears before, showed extensive diVuse reticu-lonodular
shadowing with honeycombing andperipheral and basal accentuation
(fig 1).
Physical examination revealed an afebrileemaciated women with
respiratory rate of 20breaths/min, and a blood pressure of 150/90mm
Hg (after medication). Heart sounds werenormal and there were
bilateral fine basalcrackles over the lungs. There was no
palpableperipheral lymphadenopathy or pedal oedemabut there was
clubbing of both fingers and toes.A new posteroanterior chest
radiograph was
done (fig 2). Investigations revealed mildhypochromic anaemia
and a normal white cellcount with eosinophilia of 16.4%. Her
erythro-cyte sedimentation rate was raised at 121mm/hour. Arterial
blood analysis revealed anoxygen tension of 8.96 kPa, carbon
dioxidetension 3.99 kPa, and pH 7.39. Microscopicexamination of the
sputum was negative foracid-fast bacilli.
Questions(1) What does the chest radiograph in fig 2
show?(2) Suggest two causes that would explain the
new radiological finding in fig 2.(3) What three further
investigations would
you request?(4) What is the final diagnosis and what is the
relative risk of its development in patientswith diVuse
interstitial pulmonary fibro-sis?
(5) In your opinion, what is the major riskfactor for the final
diagnosis in this case?
Al-Sabah Hospital,Kuwait: Department ofMedicineA Al-Adsani
Department ofDiagnostic Radiologyand ImagingM H Dahniya
Mansouria HealthClinic, KuwaitN Al-Adsani
Correspondence to:Dr A Al-Adsani, PO Box31098, 90801
Sulaibikhat,[email protected]
Submitted 9 June 1999Accepted 22 November 1999
Answers on p 137.
Figure 1 Chest radiograph two years before presentation.
Figure 2 Posteroanterior chest radiograph.
Self assessment questions 127
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SELF ASSESSMENT ANSWERS
Recurrent abdominal pain—the forgottencause
C1 INH deficiency:
Q1: Is always associated with peripheralangio-oedema and
urticariaFalseC1 INH deficiency is not associated with urti-caria
but the angio-oedema may be precededby a serpiginous erythematous
rash which isnon-pruritic. Peripheral angio-oedema is a
wellrecognised presentation but mucosal angio-oedema can be life
threatening and may involvethe bowel.
Q2: Symptoms can be precipitated by theoral contraceptive
pillTrueThe oral contraceptive pill and menstrual cyclehave been
linked to exacerbations of the condi-tion but the most commonly
reported precipi-tating factors are trauma, dental extraction,and
emotional stress.1
Q3: Is the most commonly describedgenetic defect of the
complement systemand is characterised by a reduction incomplement
proteins C3 and C4FalseIt is the most commonly described
geneticdefect of the complement system2 in which C4and C2 are
reduced due to the uncheckedactivity of C1, but C3 is invariably
normal.This is because C3 convertase is not generateddue to C4b and
C2b being rapidly inactivatedin the plasma.
Q4: Is inherited in an autosomal recessivemanner and usually
presents in the firstdecade of lifeFalseC1 INH deficiency may be
inherited in anautosomal dominant (chromosome 11, p11.2–q13 ),
manner where it usually appears early inlife, or acquired
presenting in the fourthdecade or later.3 Quantitative (85%)
andqualitative (15%) deficiencies of C1 INH areresponsible for the
inherited variety2 while anincreased catabolic rate and
autoantibodies toC1 INH are responsible for the two
acquiredforms.4
Q5: Is primarily treated with fresh frozenplasma which has
replaced steroids andantihistamines as the treatment of
choiceduring acute episodesFalseC1 INH concentrate is preferred for
the acuteepisode, because fresh frozen plasma containsC1 and C2
which may aggravate symptoms.
Q6: May be treated by antifibrinolyticdrugs, particularly in the
acquiredvariety or in those not responding
toandrogensTrueProphylactic treatment is by substituted andro-gens
(stanozolol) and antifibrinolytic drugs(tranexamic acid).
Antifibrinolytics are thetreatment of choice before puberty and
inwomen trying to conceive.
DiscussionAngio-oedema was originally documented byMilton in
1876,4 while Osler described heredi-tary angioneurotic oedema in
1888.5 Donald-son et al first recognised that a deficiency of C1INH
was the cause of hereditary angio-oedemain 1963.6 C1 INH is a 104
kDa protein and itsdeficiency is the most commonly describedgenetic
defect of the complement system.2 Itacts as a serine protease
inhibitor upon theC1qrs enzyme complex of the classical comple-ment
pathway as well as those of the kallikreinand plasminogen pathways.
It is believed thatangio-oedema is a result of reduced C1
INHfunction through a reduced inhibition ofkallikrein, complement
system activation, andkinin generation.7
A common presentation of C1 INH defi-ciency is that of recurrent
episodes of acute,colicky abdominal pain associated with vomit-ing.
Reports exist of patients undergoingoperative exploration in the
mistaken beliefthat a surgical emergency underlies the ab-dominal
pain.8 Findings at operation include alarge amount of serous fluid
and intestinal walloedema, which can lead to intussusception
andhypovolaemic shock. Our case was saved fromlaparotomies because
the diagnosis of “ab-dominal migraine” had been made
repeatedly.Non-mucosal angio-oedema is usually welldemarcated,
localised, and most commonlyfound aVecting skin on the extremities.
Themucous membranes of the mouth, pharynx,and larynx may be
involved.
Trauma, dental extractions, and emotionalstress are among the
most common precipitat-ing factors, while the menstrual cycle and
oralcontraceptive pill have also been linked toexacerbations of the
condition.1
Initial investigations of suspected C1 INHdeficiency should
include measurement of thecomplement components C2, C3, C4, and
C1INH. Further immunological investigations mayinclude assays for
functional C1 INH, C1, andC1 autoantibodies. If acquired C1 INH
issuspected serum electrophoresis may identifythe monoclonal
paraprotein of a B cell lympho-proliferative condition. Barium
studies duringabdominal pain may show a classical “stackedcoin
appearance”, but confirmation is achievedby quantitative and
qualitative measurement ofC1 INH.
Treatment of the acute episode is preferen-tially with C1 INH
concentrate which shouldalso be used prophylactically before
surgery.
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The use of fresh frozen plasma is controversialbecause it
contains C1 and C2, which mayaggravate symptoms.
Prophylactic treatment is by substitutedandrogens (stanozolol)
and antifibrinolyticdrugs (tranexamic acid). Antifibrinolytics
maybe eVective in the acquired variety, those notresponding to
androgens, and are indicatedbefore puberty and in women trying
toconceive. Treatment of associated conditionsmay lead to
symptomatic improvement inacquired C1 INH deficiency.
AVected individuals should wear MedicAlert bracelets. Genetic
counselling andscreening should be oVered to their families,even
those apparently not aVected, because theclinical course of the
disease can be sovaried.
The diagnosis of C1 INH deficiency isfrequently missed, as
happened in our patientover a period of 14 years. It should be
consid-ered in any case of recurrent abdominal painfor which no
obvious cause can be found.
1 Yip J, CunliVe WJ. Hormonally exacerbated
hereditaryangioedema. Aust J Dermatol 1992;33:35–8.
2 Carreer FMJ. The C1 inhibitor deficiency. Eur J Clin
ChemBiochem 1992;30:793–807.
3 Alsenz J, Bork K, Loos M. Autoantibody mediated
acquireddeficiency of C1 inhibitor. N Engl J Med
1987;316:1360–6.
4 Milton JL. On giant urticaria. Edinburgh Medical
Journal1876;22:513–26.
5 Osler W. Hereditary angioneurotic oedema. Am J Med
Sci1888;95:362–7.
6 Donaldson VH, Evans RR. A biochemical abnormality inhereditary
angioedema: absence of serum inhibitor of C1esterase. Am J Med
1963;35:37–44.
7 Cicardi M, Agostini A. Hereditary angioedema. N Engl JMed
1996;334:1666–7.
8 Cohen N, Sharon A, Golik A, et al. Hereditary angioneu-rotic
edema with severe hypovolaemic shock. J Clin Gastro-enterol
1993;16:237–39.
A rare coincidence and recurrent urinarytract infections
Q1: What is the initial diagnosis?Enterovesical fistula
secondary to bladder car-cinoma complicated by urinary tract
infection.
Common causes of enterovesical fistula are1:x Diverticular
disease of colonx Colonic malignancyx Granulomatous bowel diseasex
Iatrogenic (for example, radiation therapy)Clinical symptoms and
signs are varied, mainlyurinary tract infection (100%),
pneumaturia(66%), and faecaluria (50%).2 Awareness of
thepossibility of an enteric origin of recurrenturinary tract
symptoms should help prevent thelong delays in diagnosis.3
Cystoscopy is regarded as the most usefuldiagnostic procedures
in detecting fistula.4
Other modes of investigation are barium enema,cystography,
colonoscopy, and computed tom-ography.1 2 In this case computed
tomographydistinctly (see p 122) showed (A) gas in thebladder (B)
mass involving the bladder.
Treatment depends on the aetiology, localisa-tion, and the
patient’s general condition. Com-monly used technique is resection
of thefistulous tract and the compromised intestinalsegment,
followed by repair of the bladder.4 Theprocedure can be performed
as a single stagewhen the aetiology is diverticular or
granuloma-tous bowel disease. Staged repairs are morejudicious in
patients with a large interveningpelvic abscess or those in whom
advancedmalignancy or radiation changes are present.1
Insertion of colonic stent, laparoscopic repair,5
and use of human fibrin glue for a recurrent fis-tula have also
been described in the literature.
Q2: What and how common are thehistological
findings?Unexpectedly, pathological assessment showedthat the
fistula was formed by two distinct pri-maries: adenocarcinoma from
the colon andtransitional cell carcinoma from the bladder.Note fig
2 (see page 122): (A) colonicadenocarcinoma and (B) poorly
diVerentiatedtransitional cell carcinoma.
Malignancy is a known cause (35%–66%)2 4
of enterovesical fistula. The latter is mostcommonly
vesicosigmoidal by location(50%).4 In this case the site of fistula
wasbetween dome of the bladder and sigmoidcolon in deed. However,
occurrence of twounrelated primaries of adjacent organs at thesame
site, which collided to form a fistula, wasan extremely rare
coincidence. We have notfound any published reports of a
similarnature, which makes this case unique.
Q3: What is the prognosis?When the fistula is of malignant
origin, the longterm prognosis remains poor, as it is for
anycolonic (or bladder) carcinoma extendingbeyond the serosa and
involving a contiguousorgan. Fistulas secondary to radiation
necrosisand recurrent tumour have an extremely pooroutlook.
Patients with fistulas due to diverticu-lar disease (and to a
lesser extent, Crohn’s dis-ease) can look forward to complete
correctionwith low morbidity and mortality.3
This patient sadly died eight months afterthe operation from
distant metastases.
Final diagnosisMalignant vesicosigmoidal fistula due to
colli-sion between two distinct primary tumoursarising from the
colon and bladder respectively.
1 McBeath RB, SchiV M Jr, Allen V, et al. A 12 year
experiencewith enterovesical fistulas. Urology 1994;44:661–5.
2 Hernandez Millan I, Salinas Sanchez AS, Pastor GuzmanJM, et
al. Vesico-intestinal fistulae. Actas Urol Esp 1993;17:252–8.
3 Karamchandani MC, West CF Jr. Vesicoenteric fistulas. AmJ Surg
1984;147:681–3.
4 Alapont-Perez FM, Gil-Salom M, Esclapez-Valero JP, et
al.Acquired enterovesical fistulas. Arch Esp Urol
1994;47:973–7.
5 Puente I, Sosa JL, Desai U, et al. Laparoscopic treatment
ofcolovesical fistulas: technique and report of two cases.
SurgLaparosc Endosc 1994;4:157–60.
Learning pointsC1 esterase inhibitor deficiency:x Commonest
complement deficiencyx Significant morbidity and mortalityx Easy
and cheap to diagnosex Eminently treatablex Should be considered in
any case of
recurrent abdominal pain for which noobvious cause can be
found
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Obtunded sensorium in a trauma patient
Q1: What is the most likely cause ofdeterioration of GCS in this
case?Hypoxia is the most important preventablecause of obtunded
sensorium in a traumapatient. It may manifest in the form
ofnon-purposeful motor responses, and, there-fore, is a strong
indication for the need fordefinitive airway.1 Hypoxia and
hypotensionare to be ruled out before incriminating intrac-ranial
events or drugs (alcohol) as a cause ofdeterioration in GCS
score.
Q2: What should be the next step?Extubate the patient because
the tube isblocked. Oxygenate him with mask, and estab-lish a
definitive airway once again.
The cuV of the endotracheal tube wasimmediately deflated and the
patient was extu-bated. The oral cavity and pharynx werecleaned and
he was put on an oxygen mask. Hewas reintubated with another
endotrachealtube and ventilated. Immediately thereafter, abottle of
saline (500 ml) was infused over 15minutes. After 30 minutes of
reintubation hisblood pressure improved to 105 mm Hg systo-lic. Two
hours after reintubation and ventila-tion, his arterial blood gases
were: oxygen ten-sion 13.6 kPa, carbon dioxide tension 5.6 kPa,and
pH 7.32. About five hours after admissionhis blood pressure was 110
mm Hg and GCSscore improved to 4/10. By this time the fluidinfusion
was limited to 800 ml (since admis-sion) in view of the head injury
and lack of anyapparent blood loss (internal/external).
Q3: What is the most probable cause ofhypotension in this
case?In a trauma setting, hypoxia is the most impor-tant
preventable cause of death. Myocardialcontractility is reduced in
the presence ofhypoxia or acidosis.2 Correction of hypoxia
andacidosis (respiratory) after reintubation andventilation
resulted in improvement in bloodpressure. Only an 800 ml fluid
infusion overfive hours was needed to raise his bloodpressure; this
indicates that it was not hypovol-aemia that was the main cause of
the lowerblood pressure.
Q4: What is the finding shown in fig 1 (seep 123)?The tube is
blocked with a blood clot.
Q5: What is the most likely explanationfor the development of
blockage of thisendotracheal tube?Aspirated blood would block the
endotrachealtube. It is an important possibility in this caseas the
patient had epistaxis at the time of pres-entation to the district
hospital. Endotrachealsuctioning, during transfer, could have
savedhim from such a catastrophe.
Blocked or displaced endotracheal tubes arean important cause of
hypoxia in traumaduring transfer. Whenever a patient is shiftedfrom
one ward/hospital to other, one mustensure patency and correct
positioning3 of the
endotracheal tube. This can be easily accom-plished by a trained
paramedic.
DiscussionIt is not surprising that there is deterioration inthe
sensorium because of a blocked ordisplaced tube. What is surprising
is the lack ofawareness, and desire to take appropriatemeasures
(pre-hospital trauma care), amongthe public, administrators, and
medical profes-sionals that hypoxia can kill very quickly. Ali etal
reported much improved care after introduc-tion of the pre-hospital
trauma life supportprogram (PHTLS), on the principles ofAdvanced
Trauma Life Support.4 PHTLS hasbeen shown to be eVective when
compared tocare before introduction of PHTLS in, forexample, the
frequency of airway control(99.7% v 10%). Failure to monitor
theendotracheal tube resulted in the lumen beingcompromised by
blood clots, a preventablecomplication. The major clinical problem
inthis case is that it took three hours for thepatient to arrive at
a tertiary centre and thepatient was not accompanied by medical
orparamedical staV. Besides the medical lessonslearnt from this
case, an even more importantmessage is for planners of medical
care. Theyshould be aware that tertiary care hospitalscannot treat
patients eVectively until andunless primary and secondary care is
madeeVective. Good communication and a safeparamedical escort to a
further referral centreis the key as trauma patients with a
compro-mised airway cannot wait.
Final diagnosisHypoxia causing obtunded sensorium.
1 Subcommittee on Advanced Trauma Life Support of theAmerican
College of Surgeons Committee on Trauma1993–1997. Initial
assessment and management. Advancedtrauma life support program for
doctors. Chicago: AmericanCollege of Surgeons, 1997: 21–46.
2 Kaplan JA. Cardiovascular physiology. In Miller RD,
ed.Anaesthesia. 2nd Ed. Edinburgh: Churchill-Livingstone,1986:
1165–97.
3 Subcommittee on Advanced Trauma Life Suport of theAmerican
College of Surgeons Committee on Trauma1993–1997. Airway and
ventilatory management. Advancedtrauma life support program for
doctors. American College ofSurgeons, 1997: 75–85.
4 Ali J, Adam RU, Gana TJ. EVect of the prehospital traumalife
support program (PHTLS) on prehospital trauma care.J Trauma
1997;42:786–90.
Acute appendicitis: an unusual cause
Q1: Describe the histological featuresHistopathological
examination of the appendix(fig 1) shows deposits of adenocarcinoma
asso-ciated with acute inflammation. Examinationof the ovary (fig
2) and omentum (fig 3)confirm the presence of papillary
adenocarci-noma of the ovary with spread to the omentumas well as
the appendix.
Q2: What further treatment is indicated?Total abdominal
hysterectomy and leftsalpingo-oophorectomy (right
salpingo-oophorectomy and omentectomy having al-ready been
performed) to “debulk” the tumourmass, followed by cytotoxic
chemotherapy
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(with cisplatin and either paclitaxel or cyclo-phosphamide)1 is
indicated.
DiscussionEpithelial cancer of the ovary is characterised
byexfoliation of malignant cells and early dissemi-nation
throughout the peritoneal cavity. Theappendix is a common site of
such metastasis,both macroscopically apparent and occult,
andappendicectomy is performed by some gynae-cologists as part of
surgical staging and to reducetumour burden before chemotherapy. In
onestudy of women with epithelial ovarian tumours,39% overall and
49% with FIGO stage III (dis-ease outside the pelvis) or IV
(distant metas-tases) had appendiceal secondaries; about onethird
of these were occult (that is, microscopiconly).2 In three cases
appendices involved withtumour were found to be acutely
inflamedmicroscopically, but none of these was sympto-matic. In
another series, appendiceal metastaseswere found in 63% overall and
in 80% with stageIII or IV ovarian disease.3
The aetiology of appendicitis is not entirelyclear, but
obstruction of the lumen is thoughtto play an important part in
some cases. Thismay be due to lymphoid tissue, foreign body,or, in
an older age group, caecal carcinoma.We have found only one
previous report of acase of ovarian carcinoma presenting withacute
appendicitis.4 While metastatic ovariancancer is a very rare cause
of appendicitis,these cases emphasise the importance of thor-ough
examination of the abdomen and pelvisat appendicectomy, even in the
presence ofunequivocal appendicitis.
Final diagnosisAcute appendicitis due to metastases
frompapillary carcinoma of the ovary.
1 Ozols RF. Paclitaxel plus carboplatin in the treatment
ofovarian cancer. Semin Oncol 1999;26:84–9.
2 Ayhan A, Tuncer ZS, Tuncer R, et al. Is routineappendectomy
beneficial in the management of ovariancancer? Eur J Obstet Gynecol
Reprod Biol 1994;57:29–31.
3 Sonnendecker EW, Margolius KA, Sonnendecker HE.Involvement of
the appendix in ovarian epithelialcancer—an update. S Afr Med J
1989;76:667–8.
4 Costello C, Saxton J. Appendicitis and cancer. Postgrad
Med1951;9:482–4.
Figure 1 Histological section of appendix (haematoxylin and
eosin stain, originalmagnification × 100).
Figure 2 Histological section of right ovary (haematoxylin and
eosin stain, originalmagnification × 100).
Learning pointsx Ovarian cancer frequently spreads to
the appendix, resulting inmicrometastases.
x Metastatic ovarian cancer is a very rarecause of acute
appendicitis.
x It is important to perform a thoroughlaparotomy in adult cases
of acuteappendicitis.
Figure 3 Histological section of omentum (haematoxylinand eosin
stain, original magnification × 200).
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Is spiral computed tomography theimaging modality of choice for
renalcolic?
Q1: What is the diagnosis, and what isspiral computed
tomography?The patient was diagnosed as having left sidedrenal
colic due to a calculus in her left proximalureter. A spiral
computed tomogram allowsimaging of the entire abdomen and pelvis
dur-ing one breath hold, eliminating respiratoryartefacts. The
entire technique of performingspiral computed tomography takes
approxi-mately 30 seconds to complete.
Q2: What are the findings on the spiralcomputed tomogram?A
spiral computed tomogram of the abdomenwas performed. No
intravenous contrast me-dium was used during the procedure. It
showeda normal right renal tract. There was a 6 mmcalculus in the
proximal left ureter and an 8mm calculus in the inferior pole calyx
of the leftkidney (fig 1; see p 124). These calculi were
notvisualised in the intravenous urogram.
Q3: What are the advantages of spiralcomputed tomography in
evaluating acase of renal colic?There are several advantages in
performing aspiral computed tomogram to evaluate acuteflank pain.
As the imaging with spiral computedtomography is performed without
contrastmedium, the stones are not masked by the pres-ence of
radio-opaque contrast. With conven-tional computed tomography
stepwise slices aretaken and therefore it is possible to miss a
stone.Spiral computed tomography provides a con-tinuum profile of
the urinary tract and thereforeis unlikely to miss a stone. Like an
intravenousurogram but unlike an ultrasound scan, a spiralcomputed
tomogram gives good imaging of theureter and has the same advantage
as an intra-venous urogram to be able to delineate the levelof
obstruction. Unenhanced spiral computedtomography is reported to
have more than 95%sensitivity and specificity in the diagnosis
ofobstructing ureteral calculi. Within the next fewyears spiral
computed tomography may replaceintravenous urography in the
evaluation of renalcolic.
DiscussionIntravenous urography has been the procedureof choice
for evaluation of renal colic since itwas first performed in 1923.1
It provides struc-tural as well as functional information of
theurinary tract. In addition it gives us infor-mation regarding
the site, degree, and thenature of obstruction. There are a
fewdisadvantages with intravenous urography. Theincidence of
contrast induced allergic reactionsis 5%–10%.2 3 There is 25% risk
of contrastinduced nephrotoxicity in people with pre-existing renal
failure and diabetes mellitus.4
Intravenous urography is more time consum-ing. On the other hand
spiral computedtomography has several advantages. As theimaging
with spiral computed tomography isperformed without contrast
medium, thestones are not masked by the presence of
radio-opaque contrast. Total time taken to per-form a spiral
computed tomography is less thana minute. Like an intravenous
urogram, butunlike an ultrasound scan, a spiral computedtomogram
gives good imaging of the ureter andhas the same advantage as an
intravenous uro-gram to be able to delineate the level
ofobstruction. The sensitivity and specificity ofunenhanced spiral
computed tomography inthe diagnosis of renal colic is reported to
bemore than 95%.5–7 Evaluation of spiral com-puted tomography and
intravenous urographyrevealed comparable radiation dosages andwith
a lower gonadal dose provided by the spi-ral computed tomography.8
The main disad-vantage of unenhanced spiral computed tom-ography
compared with intravenous urographyis the absence of evaluation of
renal functionand the lining epithelium of the urinary tract.Rarely
phleboliths in the pelvis could beconfused with ureteral stones on
spiral com-puted tomography.1 Osborn ED, Sutherland CG, Scholl AJ,
et al. Roentgenogra-
phy of urinary tract during excretion of sodium iodide.JAMA
1923;80:368.
2 Shehadi WM, Toniolo G. Adverse reactions to contrastmedia: a
report from the committee on safety of contrastmedia of the
International Society of Radiology. Radiology1980;137:299–302.
3 Katayama H, Yamaguchi K, Kozuka T, et al. Adversereactions to
ionic and non-ionic contrast media. Radiology1990;175:621–8.
4 Barrett BJ, Carlisle EJ. Metaanalysis of the relative
nephro-toxicity of high and low osmolality iodinated contrast
media.Radiology 1993;188:171–8.
5 Smith RC, Rosenfield AT, Choe KA, et al. Acute flank
pain:comparison of noncontrast-enhanced CT and
intravenousurography. Radiology 1995;194:789–94.
6 Sommer FG, JeVrey RB, Rubin GD, et al. Detection of ure-teral
calculi in patients with suspected renal colic: value ofreformatted
noncontrast helical CT. AJR 1995;165:509.
7 Smith RC, Verga M, McCarthy S, et al. Diagnosis of acuteflank
pain: value of unenhanced helical CT. AJR 1996;166:97.
8 Fielding JR, Steele G, Fox LA, et al. Spiral
computerisedtomography in the evaluation of acute flank pain: a
replace-ment for excretory urography. J Urol 1997;157:2071–3.
Learning points: advantages of spiralcomputed tomographyx No
bowel preparation or contrast
medium is requiredx It requires less time than intravenous
urography. Entire technique of spiralcomputed tomography takes
approxi-mately 30 seconds
x It scans the entire abdomen and pelvisduring one breath hold,
eliminating res-piratory artefacts
x It is highly accurate in identifying thesize and location of
ureteral and renalcalculi
x Uric acid calculi could be accuratelydiagnosed
x The degree of obstruction to the kidneycan be assessed by the
severity ofhydronephrosis, perinephric, and peri-ureteral stranding
and perinephric fluidcollection indicating forniceal rupture
x In addition other abdominal organs canbe evaluated
x Radiation dosage is comparable to that ofintravenous urography
(4.6 v 4.4 rad,respectively), with a lower gonadal doseprovided by
the spiral computed tomog-raphy
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A young woman with intractablediarrhoea
Q1: What is the diagnosis?The diagnosis is a dopamine secreting
phaeo-chromocytoma. The abdominal computedtomogram (p 124) shows a
left adrenal mass(8 × 6 cm) with haemorrhagic and necroticareas. A
131I-metaiodobenzylguanidine scinti-gram showed uptake in the left
adrenal gland.
A histopathologically proved benign phaeo-chromocytoma was
resected. Immunohisto-chemical study revealed enhanced expression
oftyrosine hydroxylase and low expression ofdopamine â-hydroxylase
in the tumour. Thesefindings are consistent with the secretion
ofdopamine, as dopamine â-hydroxylase is theenzyme that synthesises
norepinephrine fromdopamine. An increased production ofdopamine and
homovanillic acid is uncommonwith benign lesions but may occur with
malig-nant phaeochromocytoma.1 Over a one weekperiod her diarrhoea
subsided. The plasma andurinary dopamine and urinary homovanillic
acidconcentrations returned to normal. Her bloodpressure one week
later was 140/80 mm Hg.
Q2: What is the cause of diarrhoea?The cessation of diarrhoea
after tumour resec-tion suggests that dopamine may cause
diar-rhoea, perhaps via D1-like receptors in thegastrointestinal
tract.2 Diarrhoea is an uncom-mon sole manifestation of
phaeochromocy-toma.3 A literature search revealed only oneother
report of dopamine secreting phaeochro-mocytoma presenting solely
with diarrhoea.4
Q3: What is the cause for remission of herhypertension?The
dopamine receptors in peripheral tissuesare of two functional
classes: D1 and D 2-likereceptor. Stimulation of postsynaptic,7
D1-likereceptors or presynaptic D2-like receptorsmay cause
vasodilatation.8 Stimulation ofD1-A receptors promotes natriuresis
and low-ers blood pressure in humans.9 A deficientrenal dopamine
formation or action may con-tribute to hypertension,10 and a
deficientdopaminergic response to salt loading mayplay an
aetiological part in patients with a saltsensitive form of
hypertension.11 D1-A recep-
tor deficient mice have been shown to havehypertension,
suggesting a hypotensive actionfrom dopamine.12 This is consistent
with thespontaneous lowering of blood pressure ini-tially and the
increase in blood pressure afterresection of dopamine secreting
phaeochro-mocytoma seen in our patient.13
Follow upTwo months after surgery she continues to
beasymptomatic. Her blood pressure is 140/80mm Hg. The urinary 24
hour catecholamines,dopamine, and homovanillic acid of thepatient,
her three siblings, and two sons werenormal. The patient and her
family are onregular follow up at the endocrinology outpa-tient
clinic.
Final diagnosisDopamine secreting benign phaeochromocy-toma.
1 Landsberg L, Young JB. Pheochromocytoma. In: Fauci
AS,Braunwald E, Isselbacher KJ, et al, eds. Harrison’s principlesof
internal medicine. 14th Ed. New York: McGraw-Hill,1998:
2057–60.
2 Marmon LM, Albrecht FE, Canessa LM, et al. Identifica-tion of
dopamine D 1A receptors in the rat small intestine. JSurg Res
1993;54:616–20.
3 Werbel SS, Ober KP. Pheochromocytoma: update ondiagnosis,
localization, and management. Med Clin NorthAm 1995;79:131–53.
4 Yasunari K, Kohno M, Yoshikawa J, et al. A dopamine-secreting
pheochromocytoma. Am J Med 1999;106:599–600.
5 Takizawa H, Narisawa R, Asakura H. Jejunal invasion
ofpheochromocytoma pathologically confirmed by endo-scopic biopsy.
Am J Med Sci 1999;371:67–74.
6 Ross EJ, GriYth DNW. The clinical presentation of
phaeo-chromocytoma. Q J Med 1989;71:485–96.
7 Yasunari K, Kohno M, Yokokawa K, et al. Dopamine DA1receptors
on vascular smooth muscle cells are regulated byglucocorticoid and
sodium chloride. Am J Physiol 1994;267:R628–34.
8 Goldberg LI. Cardiovascular and renal actions of
dopamine:potential clinical applications. Pharmacol Rev
1972;24:1–29.
9 Carey RM, Stote RM, Dubb JW, et al. Selective
peripheraldopamine-1 receptor stimulation with fenoldopam in
humanessential hypertension. J Clin Invest 1984;74:2198–207.
10 Aperia A. Dopamine action and metabolism in the kidney.Curr
Opin Nephrol Hypertens 1994;3:39–45.
11 Gordon MS, Steunkel CA, Conlin PR, et al. The role ofdopamine
in nonmodulating hypertension. J Clin EndocrinolMetab
1989;69:426–32.
12 Albrecht FE, Drago J, Felder RA, et al. Role of the D
1Adopamine receptor in the pathogenesis of genetic hyper-tension. J
Clin Invest 1996;97:2283–8.
13 Prey C, Fossti P, Fontaine P, et al. Dopamine
secretingpheochromocytoma: an unrecognized entity? Classificationof
pheochromocytomas according to their type of secretion.Surgery
1986;100:1154–62.
Box 1: Common mechanisms for loosemotions in phaeochromocytomax
Ectopic production by
phaeochromocytoma of: vasoactiveintestinal peptide (watery
diarrhoea,hypokalaemia, achlorhydria syndrome);serotonin;
somatostatin; calcitonin.
x In phaeochromocytoma as part of multi-ple endocrine neoplasia
2A and 2B syn-dromes; calcitonin, serotonin, andprostaglandin
production from medul-lary thyroid carcinoma may lead to
diar-rhoea.
x Phaeochromocytoma may be associatedwith gastrinoma of
Zollinger-Ellisonsyndrome, leading to presentation
withdiarrhoea.
Box 2: Gastrointestinal manifestationsof phaeochromocytoma5
6
x Nausea (with or without vomiting)x Constipationx Abdominal
painx Ileusx Pseudo-obstructionx Diarrhoeax Ischaemic
enterocolitisx Gastrointestinal bleedingx Cholelithiasisx Acute
abdomen with hyperamylasaemiax Hunger
Learning pointIntractable diarrhoea may be the onlymanifestation
of a dopamine secretingphaeochromocytoma
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A young man with tachycardia
Q1: What is the diVerential diagnosis?The important diVerential
diagnosis for airregular broad complex QRS tachycardia is:x Atrial
fibrillation with aberrant conductionx Atrial fibrillation with
pre-excitationx Atrial fibrillation with pre-existing bundle
branch blockx Polymorphic ventricular tachycardia
Q2: What is the most likely diagnosis?The rapid ventricular
rates and the absence ofcardiovascular risk factors should make
onesuspect atrial fibrillation with pre-excitation(conduction via
the accessory pathway). WolV-Parkinson-White syndrome was confirmed
inthis patient in the electrocardiogram takenduring sinus rhythm
after treatment.
Q3: How will you manage this patientacutely?In view of the
hypotension DC cardioversion isthe best choice.
Q4: What is the long term management?Patients with
WolV-Parkinson-White syn-drome with symptomatic arrhythmias,
particu-larly life threatening ones like atrial fibrillation,should
be referred for radiofrequency ablationfor elimination of the
accessory pathway.Flecainide, propafenone, and sotalol are
pro-phylactic antiarrhythmic drugs of choice whilethe patient is
awaiting the procedure.
DiscussionAtrial fibrillation is the second commonest(10%–30%)
arrhythmia in patients with WolV-Parkinson-White syndrome after
orthodromicatrioventricular (AV) re-entrant tachycardia(AVRT) which
is a narrow QRS regular tachy-cardia almost identical to AV nodal
re-entranttachycardia. The cardinal features of atrialfibrillation
in WolV-Parkinson-White syn-drome are the irregularity and the
rapidventricular rates as well as the varying QRSconfiguration.
Ventricular rate is an aggregateof conduction over the normal AV
node andaccessory pathways and it can approach 300 to350 beats/min.
QRS configuration is deter-mined by the route of atrial impulses
which isdependent mainly upon the refractory periodof the accessory
pathway.
If the refractory period of the accessorypathway is short, the
antegrade conductionoccurs via the accessory pathway to produce
anirregular wide QRS tachycardia as in this case,while it is no
diVerent from usual atrial fibrilla-tion if conduction takes place
via the AV node.Varying degrees of fusion beats can also befound.
Short eVective refractory period ofaccessory pathway1 and short R-R
intervalbetween consecutive pre-excited complexes2
are associated with rapid ventricular rates thatcan degenerate
into ventricular fibrillation3 andsudden death.
The pathogenesis of atrial fibrillation inWolV-Parkinson-White
syndrome is poorlyunderstood.4 5 It is more common in patientswith
multiple accessory pathways. Though the
accessory pathway is important in the patho-genesis of atrial
fibrillation, it is probably notrequired for the initiation of
atrial fibrillation6
and the accessory pathway is usually a passivebystander. However
some reports suggest thataccessory pathways are branched and can
sup-port microre-entry.
Atrial fibrillation is almost always associatedwith concomitant
inducible AVRT, and sponta-neous degeneration of AVRT into
atrialfibrillation has been reported to represent themost frequent
mode of initiation. It is unclearwhy all patients with AVRT do not
developatrial fibrillation.7 Intrinsic atrial electrophysi-ological
abnormalities5 8 and exaggerated sym-pathoadrenal discharge have
all been blamed inthe pathogenesis of atrial fibrillation.
Associ-ated abnormalities like mitral valve prolapseand Ebstein’s
anomaly9 can be found.
Electrical cardioversion is the treatment ofchoice in
pre-excited atrial fibrillation as it candegenerate into
ventricular fibrillation. How-ever if haemodynamically well
tolerated,chemical cardioversion can be tried. Thoughintravenous
flecainide, propafenone, procaina-mide, sotalol, and amiodarone
have all beenshown to be eVective in cardioverting pre-excited
atrial fibrillation or reducing theventricular rate, class Ic drugs
(flecainide andpropafenone) are popular choices. Verapamiland
digoxin are contraindicated as they blockconduction via the AV node
enhancing con-duction via the accessory pathway therebyactually
increasing the ventricular rate. Intra-venous amiodarone should be
used withcaution in pre-excited atrial fibrillation asincrease in
the ventricular rates and ventricularfibrillation have been
reported. Radiofre-quency ablation is the treatment of choice
inpatients with symptomatic arrhythmias. It isusually but not
always successful in preventingatrial fibrillation. However it will
eliminate thelife threatening rapid ventricular rates whichcan be
associated with it.
Final diagnosisWolV-Parkinson-White syndrome.
1 Wellens HJJ, Durrer D. WolV-Parkinson-White syndromeand atrial
fibrillation. Relation between refractory period ofthe accessory
pathway and the ventricular rate during atrialfibrillation. Am J
Cardiol 1974;34:777–82.
2 Pieterson AH, et al. Atrial fibrillation in
WolV-Parkinson-White syndrome. Am J Cardiol 1992;70:38A–43A.
3 Monteya PT, et al. Ventricular fibrillation in
WolV-Parkinson-White syndrome. Eur Heart J 1991;12:144–50.
4 Shakespheare CF, Anderson M, Camm AJ. Pathophysiologyof
supraventricular tachycardia. Eur Heart J 1993;14(suppl):2–8.
5 Muraoka Y, Karakawa S, Yamagata T, et al. Dependency onatrial
electrophysiological properties of appearance ofparoxysmal atrial
fibrillation in patients with WolV-Parkinson-White syndrome:
evidence from atrial vulnerab-lity before and after radiofrequency
catheter ablation andsurgical cryoablation. Pacing Clin
Electrophysiol 1998;21:438–46.
6 Wathen M, Natale A, Wolfe K, et al. Initiation of atrial
fibril-lation in the WolV Parkinson syndrome: the importance
ofaccessory pathway. Am Heart J 1993;125:753–9.
7 Bauernfeind RA, Wyndham CR, Swiryn SP, et al. Paroxys-mal
atrial fibrillation in the WolV-Parkinson-White syn-drome. Am J
Cardiol 1981;47:562–9.
8 Michelucci A, Padeletti L, Monizzi D, et al.
Atrialelectrophysiological properties of patients with
asympto-matic WolV-Parkinson-White syndrome. Eur Heart
J1988;9:479–83.
9 Pressley JC, Wharton JM, Tang AS, et al. EVect of
Ebstein’sanomaly on short and long term outcome of
surgicallytreated patients with WolV-Parkinson-White syndrome.
Cir-culation 1992;86:1147–55.
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A small axillary nodule—a therapeuticdilemma?
Q1: What is the significance of an axillarynodule in an elderly
patient?In an elderly patient, an axillary nodule may bea
metastatic deposit from a known or unknownprimary tumour. Axillary
lymph node metasta-sis other than breast cancer, especially in
males,includes lung, thyroid, gastric, colorectal, andpancreatic
malignancy; however, in females thecommonest is ipsilateral breast
cancer.1
Q2: What should be the diagnosticmodality in a case of axillary
nodule?A suspicious nodule (particularly in an elderlyperson)
should always have a histopathologicaldiagnosis by FNAC and/or
histopathology.
Q3: What is the treatment modality in acase of axillary nodule
with occultmetastasis?Once diagnosed, routine haematological
andbiochemical investigations, chest radiography,ultrasonography of
the abdomen, and bilateralmammography are undertaken.
Additionalinvestigation to locate the exact site of primarytumour
is unrewarding.2 In most of the serieson this subject, the
sensitivity of mammogra-phy in the identification of the occult
lesion isas low as 33%.3 Magnetic resonance imaging(MRI) may be
helpful; however, the absence ofabnormality on mammography and MRI
doesnot exclude the diagnosis of primary breastcancer. A bone scan
may be done as a part ofmetastatic work up.
Total mastectomy and axillary clearance arepractised by the
majority of surgeons.4 Recentlysome surgeons have suggested
conservative sur-gery with or without radiation therapy.5
Eller-broek et al treated such patients with irradiationalone and
showed a 17% five year actuarial riskfor locoregional recurrence.6
Advantagesclaimed are that the breast is preserved and sur-vival is
comparable to total mastectomy. Thepresence of extensive tumour
burden and multi-focality, even when the disease is
clinicallyoccult, may limit breast conservation therapy asit may
not be feasible to excise the primary ordeliver a boost dose of
radiotherapy to theprimary site. Moreover, in the absence of
detailsof the primary tumour and lymph nodal status,it is not
possible to evaluate tumour characteris-tics and prescribe adjuvant
treatment.
Q4: What are the various histopathologicalconsiderations in such
a case?The pathologist should be alerted to the occultprimary in
the breast as more sections may berequired to locate the tumour. A
primarytumour is identified only in 64%–93% asreported in various
series.6 Infiltrating duct car-cinoma is the commonest tumour,
while carci-noma in situ is seen in 8%–20% of cases.3 Rosenand
Kimmel reported median tumour size of 1.5cm (0.1–6.6 cm).7 Baron et
al had noted 45% oftheir cases to be multifocal.3 A study of
hormonereceptors may be helpful in confirming the diag-nosis as it
is positive in 50%–60% of the casesand a negative result does not
exclude breast
carcinoma.3 A positive result can also be seen inother
malignancies like renal cell carcinoma,melanoma, and colorectal
carcinoma.
DiscussionIn 1907, William Steward Halsted first de-scribed two
patients with extensive carcinoma-tous involvement of the axilla
caused by occultbreast cancer.8 The incidence of occult carci-noma
with axillary nodal metastasis varies from0.35% (35 out of 10 014
patients) at theMemorial Sloan-Kettering Cancer Center to0.5%
(60/12 000) at the National CancerInstitute in Milan.3
The commonest cause in females is ipsilateralbreast cancer. No
investigations can identify anoccult primary lesion with accuracy.
Totalmastectomy and axillary clearance, conservativesurgery with or
without radiation, and primaryradiation therapy are the various
options avail-able in elderly patients. Total mastectomy
andaxillary clearance are undertaken especially inpatients where
frequent follow up is not possibleand the patient does not opt for
breast conserva-tion treatment. Since studies have shown
signifi-cant survival advantage in patients with stage IIbreast
cancer after adjuvant therapy, patientswith occult carcinoma
metastatic to the axillashould be treated as stage II disease and
henceadjuvant systemic therapy instituted.
In an elderly postmenopausal patient onlytamoxifen should be
given as a treatmentoption especially in the case of an occult
orsmall oestrogen receptor positive primary.
In our patient, no primary focus could bedetected in the large
number of sections thatwere studied, although it is not possible
for usto completely rule out the presence of a smallfocus in the
unexamined parts of the breast.The axillary metastasis was in the
centre of theaxilla in the subcutaneous tissue with no meta-static
deposit found in the lymph nodes. It isdiYcult to predict whether
the tumour waspresent in ectopic breast tissue or part of
theaxillary tail or it was an occult primary in thebreast with
metastasis to subcutaneous axillarytissue. Carcinoma has also been
reported toarise primarily in the ectopic breast tissueinclusions
present in an axillary lymph node.9
Our case demonstrated metastasis in thesubcutaneous tissue, a
rare event. This casegives an important message; however small
a
Learning pointsx A small axillary nodule in an elderly
woman can be metastatic tumour.x A primary tumour is usually
found in
the breast; however, at times the pri-mary tumour may be
occult.
x Total mastectomy and axillary clearanceare undertaken in the
case of an occultprimary in the breast with lymph nodemetastasis
where frequent follow up isnot possible and the patient does notopt
for breast conservation therapy.
x At times, the primary site is not detectedeven on
histopathological examination andsuch cases remain a therapeutic
dilemma.
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small nodule may be, especially in an elderlypatient, it should
not be ignored.
Final diagnosisMetastatic axillary nodule with occult
breastcancer.
1 Patel J, NemotoT, Rosner D, et al. Axillary lymph
nodemetastasis from an occult breast cancer.
Cancer1981;47:2923–7.
2 Osteen RT, Kopf G, Wilson RE. In pursuit of the
unknownprimary. Am J Surg 1978;135:494–8.
3 Baron PL, Moore MP, Kinne DW, et al. Occult breast can-cer
presenting with axillary metastasis. Arch Surg 1990;25:210–14.
4 Iglehart JD, Ferguson BJ, Shingleton WW. An ultrastruc-tural
analysis of breast carcinoma presenting as an isolatedaxillary
adenopathy. Ann Surg 1982;196:8–13.
5 Vilcoq JR , Calle R, Ferme F, et al. Conservative treatmentof
axillary adenopathy due to probable subclinical breastcancer. Arch
Surg 1982;117:1136–8.
6 Ellerbroek N, Holmes F, Singletary E. Treatment of
patientswith isolated axillary nodal metastases from an
occultprimary consistent with breast origin. Cancer
1990;66:1461–7.
7 Rosen PP, Kimmel M. Occult breast carcinoma presentingwith
axillary lymph node metastases: a follow up study of 48patients.
Hum Pathol 1990;21:518–23.
8 Halsted WS. The results of radical operations for the cure
ofcarcinoma of the breast. Ann Surg 1907;46:1–19.
9 Walker AN, Fechner RE. Papillary carcinoma arising fromectopic
breast tissue in an axillary lymph node. Diagn Gyne-col Obstet
1982;4:141–5.
A farmer with artificial valveendocarditis
Q1: What are the most commonorganisms causing artificial
valveendocarditis? What are other lesscommon organisms should
beconsidered?The most common aetiological organism isStaphylococcus
epidermidis which accounts for29% of both early and late onset
endocarditis,followed by viridans streptococci (17%),
Sta-phylococcus aureus (14%), and enterococci(7%).1 Aerobic Gram
negative bacilli, diph-theroids including corynebacterium
Jeikeium,and fungi especially candida and asperigillusspecies
uncommon in native valve endocarditisare important causes of early
prosthetic valveendocarditis.1
Less common organisms include Coxiellaburnetii, Brucella spp,
and the HACEK group.1
Q2: How should the diagnosis beestablished?Relapsing brucella
bacteraemia after appropri-ate treatment for acute brucellosis is
an impor-tant clue for the diagnosis of brucella endocar-ditis in
patients who have prosthetic valves.2 Anepidemiological and
exposure history is essen-tial and usually helpful in the
diagnosis. Ourpatient was a farmer who kept animals likegoats in
his farm. Diagnosis depends on isola-tion of brucella from blood
culture and/or car-diac tissues. Serology is also helpful.
Thestandard tube agglutination test is sensitive andspecific. A
titre of 1:160 or more is presumptiveevidence of brucella
infection. Echocardio-graphy especially transoesophageal
echo-cardiography may be useful in detectingvegetations, prosthesis
detachment, and
perivalvular abscess. Other indications includeanaemia,
haematuria, and a high ESR.
Q3: What would be the best therapeuticapproach?Treatment for
brucella endocarditis has notbeen well established, due basically
to the lownumber of reported cases. Brucella organismsare
susceptible to a variety of antibioticsincluding aminoglycosides,
tetracyclines, chlo-ramphenicol, quinolones, macrolides, ri-fampin,
and trimethoprim-sulfamethoxazole(TMP-SMZ).3 Most patients with
brucellaendocarditis are treated with combinationantibiotics
including tetracycline, streptomy-cin, rifampin, and/or TMP-SMZ.
The bestcombination of antibiotics is not known. Someauthors
suggested a combination of doxycy-cline, rifampin, and
streptomycin,3 however theinterference of rifampin with the
anticoagulantactivity of warfarin and related drugs, and
theinconvenience of intramuscular streptomycininjection makes this
combination less attrac-tive. Prosthetic valve endocarditis caused
bybrucella is a primary indication for surgery4; ithas never been
cured with antibiotics alone. Allreported patients had combined
medical andsurgical treatment. Our patient underwentvalve
replacement four days after the start ofantibiotic treatment. The
optimal duration ofantimicrobial therapy for brucella
endocarditisis unknown. However it seems advisable toextend
antibiotic treatment for a minimum of12 weeks postoperatively. A
progressive drop inantibody titre, and a negative
mercaptoethanoltitre, points toward a bacteriological cure;patients
who have a relapse or fail treatmentpersist with high
concentrations of IgG resist-ant to mercaptoethanol.4
DiscussionBrucellosis is a zoonosis with a worldwide
dis-tribution, especially in the Mediterraneanbasin, the Arabian
Peninsula, the Indiansubcontinent, Mexico, Central and
SouthAmerica.2 It is a systemic disease, and almostevery organ can
be aVected. The infectionusually manifests itself as a febrile
syndromewith no apparent focus, chills, sweating,arthralgia, and
myalgia. About 30% of patientssuVer from some localisation, most
commonlybone and joint involvement.1 Brucella endo-carditis is rare
occurring in fewer than 2% ofpatients with brucellosis.1 Prosthetic
valveendocarditis caused by brucella species is veryrare. Brucella
abortus, B suis, and B melitensishave been reported to cause
endocarditis.Brucella endocarditis produces highly de-structive
lesions of the valve structure.5 It usu-ally involves a previously
healthy native valve.The aortic valve is involved in more than
75%of cases. Mitral involvement occurs morerarely and usually
aVects a previously dam-aged valve.5 The valvular lesions have
beendescribed as bulky and ulcerative with grossabscesses of the
myocardium, microabscesseswithin the cusps, destruction of
commissures,and calcifications.6 These observations might
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explain the high fatality rate for brucella endo-carditis.
Although the mortality rate forbrucellosis is less than 1%,
endocarditisaccounts for 80% of these deaths.6 Thecomplication,
which is responsible for themajority of deaths, is heart failure.6
Major sys-temic emboli in contrast to other causes ofprosthetic
valve endocarditis were rare; thishas been attributed to the
tendency ofinfection to cause fibrosis, hyalinisation,
andcalcification, rather than large vegetations.2 6
Diagnosis depend on isolation of brucellafrom blood culture or
cardiac tissue, which arepositive in 80% of cases. Combined
antibioticand surgical treatment is the best approach fortreating
brucella prosthetic valve endocarditisas the mortality rate is less
than for medicaltreatment alone, and infection of the newprosthesis
that has been placed is low.1
Final diagnosisBrucella prosthetic valve endocarditis.
1 Threlkeld MG, Cobbs CG. Infectious disorders of
prostheticvalves and intravascular devices. In: Mandel GL, Douglas
RG,Bennet JE, eds. Principles and practice of infectious
diseases.Edinburgh: Churchill Livingstone, 1990: 706–15.
2 Fernandez-Guerrero ML. Zoonotic endocarditis. Infect DisClin
North Am 1993;7:135–41.
3 Mortensen JE, Moore DG, Clarridge JE, et al.
Antimicrobialsusceptibility of clinical isolates of brucella. Diagn
MicrobiolInfect Dis 1986;5:163–9.
4 Fernandez-Guerrero ML, Martinell J, Aguado JM, et
al.Prosthetic valve endocarditis caused by Brucella melitensis:a
report of four successfully treated with tetracycline,
strep-tomycin, and sulfamethoxazole and trimethoprim plus
valvereplacement. Arch Intern Med 1987;147:1141–3.
5 Colmenero JD, Reguera JM, Martos F, et al.
Complicationsassociated with Brucella melitensis infection: a study
of 530cases. Medicine (Baltimore) 1996;75:195–211.
6 Peery TM, Belter LF. Brucellosis and heart disease: II.
Fatalbrucellosis. Am J Pathol 1960;36:673–97.
Loss of weight in a female heavy smokerwith diVuse interstitial
pulmonaryfibrosis
Q1: What does the chest radiograph in fig2 (see p 127) show?In
addition to the diVuse interstitial pulmonaryfibrosis (DIPF), there
is an irregular left upperlobe opacity and apical pleural
fibrosis.
Q2: Suggest two causes that wouldexplain the new radiological
finding in fig2 (see p 127)Pulmonary tuberculosis and lung cancer
arethe two most likely causes of an opacity in theupper lobe of the
lung.
Q3: What three further investigationswould you request?Sputum
culture for acid-fast bacilli, sputumcytology for malignant cells,
and high resolu-tion computed tomography of the chest.
Sputum culture showed mycobacteriumtuberculosis that was
sensitive to rifampicin,ethambutol and streptomycin, but resistant
toisoniazid. Sputum cytological examination ofthree specimens
revealed squamous cell carci-noma. High resolution computed
tomographyconfirmed DIPF with honeycomb reticulationand ground
glass opacity. A large irregular
cavitating mass was apparent in the anteriorsegment of the left
upper lobe (fig 3 below).
Q4: What is the final diagnosis and whatis the relative risk of
its development inpatients with diVuse interstitialpulmonary
fibrosis?Lung cancer with DIPF. It is well establishedthat the
occurrence of lung cancer is greatlyincreased in patients with
DIPF.1 2 There is anexcess relative risk of 14.1 of lung cancer
inpatients with DIPF compared with the generalpopulation of
comparable age and sex.3 Thedevelopment of lung cancer in DIPF
seems tobe related to DIPF itself, apart from smokingand no
predicting factors for its developmentin the presence of DIPF have
been identified.3
Lung cancer in this setting occurs predomi-nantly in males, in
smokers, in the lower lobes,and in the peripheral regions of the
lung.2
Q5: In your opinion, what is the majorrisk factor for the final
diagnosis in thiscase?Cigarette smoking is the most important
singleaetiological factor in the development of lungcancer. The
patient was an elderly women whosmoked heavily for more than 50
years, andhad a longstanding history of DIPF. Thesquamous cell
carcinoma she developed was inthe left upper lobe and was most
probably theresult of her heavy smoking. Her DIPF mayhave been a
contributory factor.
Clinical courseThe patient was considered unfit for
surgicalexcision or therapeutic irradiation of herneoplasm, because
of her pre-existing pulmo-nary fibrosis. She failed to respond to
aquadruple regimen of antituberculous therapy(including rifampicin,
pyrazinamide, ethambu-tol, and ciprofloxacin; streptomycin was
notprescribed because she had renal impairmentduring her illness).
She died 3.5 months afteradmission. There was no necropsy.
Figure 3 Computed tomography showing a large irregularcavitating
mass in the anterior segment of the left upperlobe.
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DiscussionAlthough the association of lung cancer andDIPF is
well established,3–5 little attention hasbeen given to it. In
comparison with the generalpopulation of lung cancer patients, lung
cancerassociated with DIPF occurs more commonlyin males, and in
smokers, and is predominantlylocated in the lower lobes and
peripheralregions of the lungs.2 The precise role of DIPFas a
predisposing factor for lung cancer isspeculative. The fact that
lung cancer occursmore frequently in the lower lobes where
fibro-sis is predominant supports the view that fibro-sis and
carcinoma are closely related. Bronchialsquamous metaplasia as a
precancerous state inDIPF is well recognised.2 Transition
fromatypical squamous metaplasia to carcinomaand anatomical
correlation between sites offibrosis and the carcinoma has been
demon-strated in some instances.1
The simultaneous occurrence of lung cancerand pulmonary
tuberculosis has been reported
by several authors.6–10 In a review of associatedlesions in
patients with lung cancer,11 pulmo-nary tuberculosis was the most
frequent lesion,followed by scars, emphysema, and thickenedpleura.
A firm aetiological relationship betweenlung cancer and pulmonary
tuberculosis hasnot, however, been established and recentanalyses
suggest that the association may becoincidental. When lung cancer
does coexistwith pulmonary tuberculosis, the diagnosis istypically
delayed.7–10
Final diagnosisLung cancer with diVuse interstitial
pulmonaryfibrosis and pulmonary tuberculosis.
1 Fraire AE, Greenberg SD. Carcinoma and diVuse
interstitialfibrosis of lung. Cancer 1973;31:1078–86.
2 Mizushima Y, Kobayashi M. Clinical characteristics of
syn-chronous multiple lung cancer associated with
idiopathicpulmonary fibrosis. A review of Japanese cases. Chest
1995;108:1272–7.
3 Turner-Warwick M, Lebowitz M, Burrows B, et al.Cryptogenic
fibrosing alveolitis and lung cancer. Thorax1980;35:496–9.
4 Callahan WP, Sutherland JC, Fulton JK, et al. Acute
diVuseinterstitial fibrosis of lungs. Arch Intern Med
1952;90:468–82.
5 GriYn JP. Interstitial pulmonary fibrosis and cancer.
Chest1995;108:1193.
6 Sakai T, Ikeda T, Nishimura Y, et al. A case of
coexistentbronchogenic carcinoma with pulmonary
tuberculosis.Kekkaku 1992;67:409–12 [abstract].
7 Fujisawa N, Nagao R, Kimoto K, et al. Study of two cases
ofactive pulmonary tuberculosis complicated by lung cancer.Kekkaku
1994;69:323–8 [abstract].
8 Martinez ME, Aparicio UJ, Cordero RP, et al. Coexistenceof
bronchogenic carcinoma and active pulmonary tubercu-losis. Arch
Bronchoneumol 1995;31:32–4 [abstract].
9 Nonaka M, Kadokura M, Tanio N, et al. Surgical problem oflung
cancer with coexisting acute pulmonary tuberculosis.Kyobu Geka
1995;48:1019–24 [abstract].
10 Svane S. Simultaneous pulmonary tuberculosis and bron-chial
cancer. A diagnostic pitfall. Tidsskr Nor
Laegeforen1996;116:1318–19 [abstract].
11 Dacosta NA, Kinare SG. Association of lung carcinoma
andtuberculosis. J Postgrad Med 1991;37:185–9.
Learning pointsx The association of diVuse interstitial
pulmonary fibrosis and lung cancer iswell established
x Lung cancer associated with DIPFoccurs more in males, in
smokers, in thelower lobes, and in the peripheralregions of the
lung
x Cigarette smoking acts as an additiverisk factor for the
development of lungcancer in patients with DIPF
x Clinical and radiological screening isimportant in patients
with DIPF
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