Pete Gorman

Physician Associate
 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
 Term ‘ Acute abdomen‘ represents rapid onset of severe abdominal
symptoms

 May indicate life-threatening intra-abdominal or on occasion extra

abdominal pathology

 Pain is usually but not always a feature

 Pain-free acute abdomen is more likely in the elderly, in children

and in the third trimester of pregnancy

 The numerous potential causes, numerous organs within the

peritoneal cavity and the potential for referred pain make definitive
diagnosis difficult

 Abdominal pain Ranks in the top three presenting complaints to

emergency departments, but only a few of those patients will have
an acute abdomen
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.
 Confusion/impaired consciousness
 Signs of shock(hypotension/tachycardia)
 Systemically unwell/septic-looking
 Signs of dehydration
 Rigid abdomen
 Patient lying very still or writhing
 Absent or altered bowel sounds
 Associated testicular pathology
 Marked involuntary guarding/rebound tenderness
 Tenderness to percussion
 History of haematemesis/melaena or evidence of latter on PR
 Suspicion of a medical cause for abdominal pain
Cardiovascular
Inferior myocardial infarction
Pericarditis
Respiratory
Lower Lobe pneumonia
Pulmonary Embolism –pleurisy
Gastrointestinal
Hepatitis
IBD
Genitourinary
Pyelonephritis
Haematological
Sickle Cell crisis
Endocrine
Diabetic Ketoacidosis
HONK
Pharmacological
opiate withdrawal,
Infective
Typhoid
HIV Associated Lymphadenopathy
Rare
Acute Intermittent Porphyria
 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
 What does you diagnostic brain think of ?
 What condition(s) may this be?
 What tests would you order?
 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?
 Urine dip : positive for Ketones, glucose and nitrites
 BMG : 13 (formally confirmed with plasma glucose)
 U/Es:
 Urea 15
 Creatinine 150
 K+ 4
 Na+ 133
 WCC : 15 (why elevated?)
 CRP: 30
 ABG: (what does it show? why is C0₂ low ? )
 Pa0₂ 13
 C0₂ 4
 PH 7.25
 Bicarbonate 18
 Chloride 93
 Blood Ketones 5 (Ketones increased)
 CXR: NAD
 ECG: (sinus tachycardia),
 ABX NAD
 Blood cultures sent (why?)
 Sputum samples sent (why?)
 Stool cultures sent (why?)
 Trop T initial 3 (why sent ?)
 We should work out the anion gap and
plasma osmolality why?
 Work it out for this patient?

 Formulae:
 Anion gap = (Na⁺ + K ⁺ ) – (HCO3⁻ + Cl ⁻)
 (133+4) - (18+93)
 Answer = ?
 26

 Anion gap is elevated at >13 mmol/L in DKA.

Plasma osmolality =

2 ([Na mmol/L] + [K mmol/L]) + [Urea mmol/L] + [glucose m mol/L].

= 2 (133+ 4) + 15 + 13
= 302

 Should be higher than 290 mOsm/Kg in cases of DKA.

 If it is higher than 320 mOsm/kg and there is not

significant ketonaemia/ketonuria, then HONK may be
the diagnosis.
What is the Diagnostic triad of DKA ?

1)Hyperglycaemia: plasma glucose>11

2)Ketones: blood ketones ≥ 3

or urinary ketones > 2+

3)Acidosis: Venous pH <7.3 or bicarbonate <15

What are the precipitants of DKA?
The four I’s

Infection (search for cause)

Infarction

Insufficient Insulin

Iatrogenic –Corticosteroids, diuretics, surgery

 See local DKA pathway
 IV Insulin (fixed rate 0.1 unit/kg/hr),but don’t stop LA
insulin (levamir and glargine)
 IV fluids ( sodium chloride with potassium chloride if
indicated)
 Monitor Potassium 2 hourly initially and adjust
potassium additive AP-Pathway
 Avoid Iatrogenic hypoglycaemia (when BM< 14 mmol/l
start 10% dextrose over 8hrs via separate line
 Escalate to ITU if: drowsy/aspiration risk, hemodynamic
compromise, young adult/risk of cerebral oedema, very
elderly, pregnant, or evidence of severe DKA.
 Severe DKA (blood ketones >6, Bicarb <5, pot <3.5 and
anion gap greater than 16). On admission!
 On basis of information about this case
should this patient be managed in ITU ?

 According to local pathway Yes as:

 Young adult greater risk of cerebral oedema

 Anion Gap >16

 55 year old male presented with sudden
onset severe unremitting pain in his
epigastrium
 Duration 60 minutes
 Associated with nausea and sweating
 PMH
 Diabetes
 HTN
 Obesity
 What are your thoughts so far?
 OBS :Temp 36,HR 115, BP 100/58, RR 20,
Sats 97% (air)
 General :Appeared pale and sweaty, JVP
raised
 Abdominal examination : unremarkable,
could not elicit tenderness ,BS +
 Auscultation of the chest :Showed basal
crepitations
 What is your differential diagnosis?
 What investigations would you order?
ST elevation in II, III and aVF.
Q-wave formation in III and aVF.
Reciprocal ST depression and T wave inversion
in aVL
ST elevation in lead II = lead III and absent
reciprocal change in lead I (isoelectric ST
segment) suggest a circumflex artery occlusion
 Initial Troponin was 150

 What is your diagnosis?

 Inferior STEMI

 What are you going to do now?

 STEMI transfer sheet PCI

 In meantime
 Give MONA if not given
 Beta Blocker and ACE (under specialist guidance)
 Cannula left hand
 Cardiac Monitor
 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.
 PMH depression, previous incidents of
pharmacological and physical DSH.
 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
 What is your differential diagnosis?

 What further questions might you ask?

 What investigations would you undertake?

 FBC normal
 Serum electrolytes sodium 130
 Urea and creatinine normal
 LFT’s normal
 Urinalysis Showed a few erythrocytes and was
negative for nitrites
 US abdomen unremarkable
 CT abdomen Showed a mild ileus
 You are called by the nursing staff to observe
the urine in the patients Foley catheter which
had turned a deep red colour.

 Have you modified your diagnosis?

Analysis
 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
 Back to you!
 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.
 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

Regency Crisis
1778
 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
 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
 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
 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.
 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.
 Acute Intermittent Porphyria,Mubashir A. Shah, MD Roderick
Remoroza, MD .Khalid Aziz, MBBS, MRCP(UK), MRCP(Ire), FACG
www.turner-white.com Hospital Physician February 2002
 Patient .co .uk . Acute Intermittent Porphyria
 Patient .co .uk . Diabetic Ketoacidosis
 Longmore,wilkinson ,Turmezei, Oxford handbook of clinical
medicine. 7th edn,oxford university press 2007
 Be gentle with me please !