A ppt for both under and post grad for MBBS, especially, in gen surgery. with clinical scenarios and tips for exams.

2. DR. NADIR MEHMOOD
Prof of Surgery
Rawalpindi Medical University

3. Contents
Overview of the acute abdomen presentation
and the pitfalls of diagnosis
・Overview of region related abdominal
pathology
・Revisiting the RED FLAGS
・A look at the potential medical causes
・3 interactive case studies
・Questions

4. OBJECTIVES
Identify clinical featuresthat help to
distinguish surgical fromnon-surgical
acute abdomen
Discuss the differential diagnosisof
acute abdomenincluding medical
causes
Construct anapproach to evaluation
and management of acute surgical
abdomen

5. Acute Abdomen
General name for presence of symptoms and
signs of inflammation of peritoneum (abdominal
lining)

6. Acute Abdomen
・Challenge to Surgeons
・Most common cause of surgical emergency
admission
・Encompass various conditions ranging from
the trivial to the life-threatening
・Clinical course can vary from minutes to hours,
to weeks
・It can be an acute exacerbation of a chronic
problem e.g. Chronic Pancreatitis, Vascular
Insufficiency

7. ACUTE ABDOMEN
• Determining exact cause is irrelevant in pre-
hospital care
• Important factor is recognizing acute abdomen is
present

8. ME
DICALCONDITIONSWITHACUTEABDOME
N
• Degenerative disease of thoracic
spine, herpeszoster, lobar
pneumonia, pleurisy,MI.
Referred pain
• Sickle cell crisis.
Haematological
• T
abesdorsalis, Henoch–Schonlein
purpura.
Infective and
inflammatory
• Uraemia,hypercalcaemia,
diabeticketoacidosis,
Addison’sdisease,acute
intermittent porphyria.
Endocrine and
metabolic

9. DIFFE
R
E
NTIALDIAGNOSISOFACUTEABDOME
N
• Acute appendicitis
• Intestinal obstruction
• Perforatedpepticulcer
• Diverticulitis
• Inflammatory bowel disease
• Acute exacerbationof peptic
ulcer
• Gastroenteritis
• Mesentericadenitis
• Meckel’sdiverticulitis
Gastrointestinal

10. DIFFE
R
E
NTIALDIAGNOSISOFACUTEABDOME
N
• Acute Cholecystitis
• Cholangitis
• Hepatitis
• Biliary colic
Liver and
biliary tract
Cholecystitis
• Acute pancreatitis
P
ancreas
• Splenic infarct and
spontaneousrupture
Spleen

11. DIFFE
R
E
NTIALDIAGNOSISOFACUTEABDOME
N
INCLUDING ME
DICALCAUSE
S
• Cystitis
• Acute pyelonephritis
• Uretericcolic
• Acute retention
Urinary tract
• Ruptured ectopicpregnancy
• T
orsionof ovarian cyst
• Ruptured ovariancyst
• Salpingitis
• Severedysmenorrhoea
• Mittelschmerz
• E
ndometriosis
Gynaecological

12. DIFFE
R
E
NTIALDIAGNOSISOFACUTEABDOME
N
• Ruptured aortic aneurysm
• Mesenteric embolus
• Mesenteric venousthrombosis
• Ischaemic colitis
• Acute aortic dissection
Vascular
• Primary peritonitis
• Secondary peritonitis
Peritoneum
• R
ectus sheath haematoma
Abdominal wall
• Haemorrhage, e.g. anticoagulants
R
etroperitoneal

13. E
VALUATION AND MANAGE
ME
NT OFACUTESURGICAL
ABDOME
N
• e.g. ruptured abdominal aortic
aneurysm.
Immediate operation
– these patientswill
die unlesstakento
theatre immediately
• may present with an acute abdomen and require urgent
operation;e.g. P
eritonitis due to P
erforated Duodenal
Ulcer or perforated appendix; however,
• preoperative dehydration and electrolyte abnormalities
need to be corrected
• before going to theatre.
Preoperative
preparationand
operationurgently
within 6 h – elderly
patients
• patients, may be dealt with ona routine emergency list,
e.g. acute appendicitis, small bowel obstruction with no
adverse symptoms (e.g. no fever, no leukocytosis, no
peritonism).
Urgent operation
(within 24 h) –
certain conditions,
particularly in
young

14. General care of the patient
• Correction of circulating volume and electrolyte imbalance.
• Central venous catheterisation and pressure monitoring
• Plasma protein depletion may also need correction
• Intravenous feeding (‘hyperalimentation’ or ‘total parenteral nutrition’) is
required.
• Gastrointestinal decompression.
• If the abdomen is soft and not tender, and bowel sounds return, oral feeding may
be progressively introduced.
• It is important not to prolong the ileus by missing this stage.

15. DIAGNOSTIC AIDS
• HISTORY/ CLINICAL EXAM
• CP ESR, CRP
• X-RAYS- CHEST AND ABDOMEN
• U/S ABD AND CT SCAN
• PERITONEAL DIAGNOSTIC ASPIRATION
C/S,R/E, AFB STAIN
• SERUM AMYLASE

16. TREATMENT
GENERAL CARE OF THE PATIENT
Correct fluid and electrolyte
Insert NG rube
Broad spect abs
Analgesics
Vital systems support
SPECIFIC TREATMENT OF THE CAUSE
OPERATIVE TREAT WHEN APPROPRIATE

17. ┃Management should focus on careful assessment to reach a differential
diagnosis list
┃Close attention should be paid to history, symptoms and signs
┃Non surgical causes as well as surgical must be considered
┃Clinical scenario can change rapidly and conclusions previously reached
by you or your colleagues may need to be revised as events evolve
┃Failure to be open-minded and review a previous diagnosis is often at
the heart of medico-legal claims relating to patients with an acute
abdomen.
┃This presentation will concentrate on diagnosing some important
medical causes in the acute setting.

18. 17 year old female
・Presented with a 2 day history of nausea, vomiting, severe abdominal pain,
thirst and increased frequency and volume of urination
・Family had eaten take out Chinese food 3 days earlier but no other member of
the family had similar symptoms
・On Examination
・Temp 36.5, HR 96, BP, 85/62, RR 29, Sats 96% on air.
・Clinically dehydrated
・Cardiovascular and respiratory examination normal
・Abdomen was diffusely and severely tender.
・She had no documented significant medical history and took no regular
medication

19. What does your diagnostic brain think of ?
・What condition(s) may this be?
・What tests would you order?

20. The nurses are concerned that the patient is breathing rapidly and
report a sickly acetone smell on the patients breath.
・The patient is very thin and family report that she has never
thrived compared to siblings
・Further thoughts ???
・Why could the patient be breathing so rapidly?
・What investigations might you do and why?

21. 18 year old female presented to A/E with 5 day history of severe abdominal pain.
・Located in epigastric and umbilical region
・Intermittent and severe in nature
・Associated with nausea and vomiting (not hematemesis)
・Denied dysurea, increased urinary frequency, chills ,fevers or change in bowel habit.
・She was not sexually active and it was the first day of menstruation.
・Periods tended to be irregular
・She had had previous admissions for severe abdominal pain associated with menstruation and a
mild hyponatraemia was noted.
・No cause had been found.

22. PMH depression, previous incidents of pharmacological and physical therapy.
・Medication
Citalopram, tetracycline (for acne)
・Observations temp 37.5, HR 110, BP 138/77, RR 20, Sats 97% air.
・Abdominal examination showed reduced bowel sounds, tenderness on deep palpation
in periumbilical region.
・Pelvic exam revealed a normal cervix and no adnexal tenderness
・PR normal no blood
・Neurological Examination
・Showed hypo-reflexia

23. What is your differential diagnosis?
・What further questions might you ask?
・What investigations would you undertake?

24. FBC normal
・Serum electrolytes sodium 130
・Urea and creatinine normal
・LFT｡ｦs normal
・Urinalysis Showed a few erythrocytes and was negative
for nitrites
・US abdomen unremarkable
・CT abdomen Showed a mild ileus

25. You are called by the nursing staff to observe the urine
in the patient’s Foley catheter which had turned a
deep red colour.
・Have you modified your diagnosis?

26. Unexplained hyponatraemia,notable urinary discolouration and
recurrent abdominal pain associated with menstruation.
・Suggestive of Acute Intermittent Porphyria (AIP)
・A fresh urine sample protected from light was sent to test for
amino laevulininic acid and porphobilogen. It was positive for
both

27. What are the other clues to diagnosis in this case?
・Mental health history
・Tachycardia,
・HTN
・Hypo-reflexia
・What other potential precipitating factors are notable in the
patient history?
・Tetracycline, menstruation.

29. Hypertension (31%)
・Tachycardia caused by release of catecholamine's (80%)
・Shock
・Postural Hypotension/collapse
・Hyponatraemia (secondary to SIADH)
・Hypokalaemia
・Hypotonia/hyporeflexia
・Proteinurea
・Red coloured urine (light dependent polymerization reaction) (25%)
・Abdominal pain (80%)
・Constipation (50%)
・Nausea and vomiting (50%)
・Psychosis/agitation/ depression/mania/hallucinations
・Peripheral neuritis
・Paralysis
・Seizures (secondary to hyponatraemia)
・Pyrexia (16%)
・Sensory impairment
・Visual disturbance

30. One of a group of rare genetic disorder (1/100-1000)
・More common in females
・Caused by errors in pathway of haem biosynthesis
・Leads to toxic accumulation of porphyrin precursors
(porphobilogen and amino
laevulininic acid).
・It is postulated that these precursors are neurotoxins
・Leads to neuro-visceral symptoms and crisis
・Autosomal dominant inheritance (qualify)
・Diagnosis by presence of porphyrin precursors in urine

31. These are legion however here are a few:
・Menstruation
・stress
・Alcohol
・Crash Diet
・Anaesthetic agents(barbiturates, halothane)
・Antibiotics (tetracyclines, sulfonamides,chloramphenicol )
・Analgesics (pentazocine)
・Oral hypoglycaemics
・Contraceptive pill

32. Get senior and expert help
・Remove any precipitants if possible
・IV fluids to correct electrolyte imbalance
・High carbohydrate intake(NG if required) WHY?
・Prescribe with care see www.uq.edu.au/porphyria
・IV haematin is treatment of choice in most centres now (How does
this work?)
・Control nausea with prochlorperazine
・Pain control with asprin dihydrocodiene or morphine
・Seizures treated with Diazepam
・Tachycardia and Hypertension with propanolol
・Recomend Medi Alert bracelet

33. Porphyrins are bi -products of intermediates in the heme biosynthetic pathway
・The precursors glycine and succinyl coenzyme A are converted to
aminolevulinic acid (ALA) in a reaction catalyzed by ALA synthetase
・This reaction is considered the rate-limiting step in heme biosynthesis and is subject to
feedback regulation by heme, the end product of the pathway.
・Two molecules of ALA combine to form porphobilinogen. Only protoporphyrin is used in
heme synthesis.
・The other porphyrins (eg, uroporphyrin, coproporphyrin) have no physiologic function
and must be excreted. Their fluorescent properties and reduced clearance account for the
diagnostic appearance of urine in some patients.
・AIP results from partial deficiency of PBG deaminase, leading to accumulation and excess
urinary excretion of toxic porphobilinogen and ALA.

34. High doses of glucose (400 g/d) can inhibit heme synthesis and
are useful for treatment of mild attack by reducing the
production of toxic porphyrin precursers (ALA and
porphobilogen).
・Intravenous heme therapy is also effective in managing acute
attacks.
・Heme is taken up by hepatocytes, in which it causes negative
feedback for the activity and synthesis of ALA synthase the
rate-limiting enzyme. Less ALA synthetase= less toxic
precursers.
・Early heme therapy for acute attacks is advocated and is
associated with improved outcomes as measured by length of
hospitalization.

35. ASSESMENT
・A Full history
・Thorough physical examination
Diagnosis can be made most of the time by
a good history and a proper physical examination.
- An exact diagnosis often impossible to make after the initial
assessment, and often relying on further investigation

55. THANK YOU