Adapted from source

 Definition
 SIRS/Sepsis
 Approach to Acute Abdomen
 Common Causes
 Case studies
 Contacting Surgical Resident
 DEFINITION:
 refers to signs and symptoms of abdominal pain and tenderness, a
clinical presentation that often requires emergency surgical therapy

 This challenging clinical scenario requires a thorough and

expeditious workup to determine the need for operative
intervention and to initiate appropriate therapy
 Many diseases, some of which are not surgical or intra-
abdominal, can produce acute abdominal pain and
tenderness
 Therefore, every attempt is made to make a correct
diagnosis so that the chosen therapy, often a laparoscopy
or laparotomy, is appropriate
(All SIRS/Sepsis related)

 Acute Appendicitis
 Acute Pancreatitis
 Acute Cholecystitis
 Acute Diverticulitis

 Others
 Obstruction, Ulcer perforation, Trauma related, Intestinal ischaemia and infarction,
Biliary colic, Renal colic, AAA, Ruptured ectopic, Meckel's diverticulitis, Boerhaave's
syndrome, volvulus, Incarcerated/strangulated hernias, Inflammatory bowel
disease, Gastrointestinal malignancy, Intussusception, Ovarian torsion, Testicular
torsion
 Nonsurgical include – uraemia, diabetic crisis, addisonian crisis, acute intermittent
porphyria, acute hyperlipoproteinemia, hereditary Mediterranean fever, sickle cell
crisis, acute leukaemia, other blood dyscrasias, lead and other heavy metal
poisoning, narcotic withdrawal, black widow spider poisoning
1. Systemic Inflammatory Response Syndrome
(SIRS)

2. Sepsis

3. Severe Sepsis

4. Septic Shock
 Caused by mediators (cytokines, enzymes, and
oxygen radicals) released from lymphocytes,
macrophages, granulocytes, and vascular
endothelial cells

 Presence of 2 or more of following:

 Temp > 38°C or < 36°C
 Pulse > 90bpm
 Respiratory rate > 20 breaths per min
 WCC > 12 or < 4 or > 10% band forms
 SIRS plus suspected or confirmed infection
 In most cases of sepsis the invading organisms are
bacteria, but sepsis can also occur in patients with
infections caused by fungal, viral, and parasitic
pathogens
 SIRS plus infection plus hypotension
with evidence of organ dysfunction
 Lacticacidaemia, oliguria, and a depressed level of
consciousness
 Hypotension responds to IV fluids
 SIRS plus infection plus organ
dysfunction plus hypotension persisting
despite fluid resuscitation
 Patients need an IV infusion of vasoactive drugs
to restore perfusion pressure
 Organ dysfunction in patients in septic shock may
progress to organ failure
 Systolic blood pressure < 90mmHg
 Fall of blood pressure of > 40mmHg
 Mean arterial blood pressure < 65mmHg
 30% or greater drop in mean arterial pressure
 Septic Shock Mortality
40 – 55%

Systemic Inflammatory
Response Syndrome Mortality
(SIRS) Severe Sepsis 15 – 25%

Sepsis Mortality
10 – 15%
 Resuscitation

 Source Control

 Antibiotics
 IV fluids
 Monitoring
 Invasive haemodynamic
 Cardiac
 Urine output
 Inotropic support
 Oxygen +/- intubation and ventilation
 Glycaemic control
 Acid/base status
 Adrenal support
 Crystalloid fluid challenge of 30mls / Kg over 30
minutes
 Requires large bore central administration (ideally)
 CVL
 Femoral line

(Average 80 Kg person 2.4L in 30 mins!)

 Drainage

 Debridement

 Resection
Biliary/Gastrointestinal Sepsis:
 IV Ampicillin 2g q6h
 IV Gentamicin daily
 IV Metronidazole 500mg tds
(Also Intraabdominal sepsis,
diverticulitis, perianal
abscess)
Acute Cholecystitis:
 IV Ampicillin 1g q6h
 IV Gentamicin daily
Ascending Cholangitis:
 IV Ampicillin 1g q6h
 IV Gentamicin daily
 + IV Flagyl if History of
biliary surgery or obstruction
Skin Source Sepsis:
 IV Flucloxacillin 2g q6h
(severe Diabetic Foot Ulcer infection
– IV Timentin 3.1g q6h)
Urinary Sepsis:
 IV Ampicillin 2g q6h
 IV Gentamicin daily
Intravascular Device Sepsis:
 IV Flucloxacillin 2g q6h
 IV Gentamicin daily
Golden hour!
 A detailed and organized history is essential to
formulating an accurate differential diagnosis and
subsequent treatment regimen
 Modern advances in imaging cannot and will never
replace the need for a skilled clinician's bedside
examination
 Pain
 NILDOORCARF
 Associated symptoms
 Nausea, vomiting, anorexia, constipation, diarrhoea, pruritus,
melena, hematochezia, hematuria, dysuria, frequency, urgency,
fevers, sweats, shakes
 Past medical/surgical history
 History of medications
 Gynaecologic history of female patients
 Social History
 Alcohol, smoking, travel
 An organized and thoughtful physical examination is critical to the development of an accurate differential diagnosis
and the subsequent treatment
 A skilled clinician will be able to develop a narrow and accurate differential diagnosis in most patients at the
conclusion of the history and physical examination
 physical examination always begins with a general inspection of the patient, followed by inspection of the abdomen
itself
Abdomen
 Inspection
 contour of the abdomen
 scars present
 hernias
 Ecchymosis, erythema or oedema of skin
 Auscultation
 quiet
 hyperactive bowel sounds
 high-pitched “tinkling” sounds
 Percussion
 gaseous distension of the bowel
 free intra-abdominal air
 degree of ascites
 presence of peritoneal inflammation
 Palpation
 Palpation provides more information than any other single component
 severity and exact location of the abdominal pain
 organomegaly or an abnormal mass lesion
 Involuntary/voluntary guarding
 Testicles in men
 Digital rectal examination
 Pelvic examination is included in all women when evaluating pain located below the umbilicus
SIGN DESCRIPTION DIAGNOSIS/CONDITION

Aaron sign Pain or pressure in epigastrium or anterior chest with persistent firm pressure applied to McBurney's point Acute appendicitis

Bassler sign Sharp pain created by compressing appendix between abdominal wall and iliacus Chronic appendicitis

Blumberg's Transient abdominal wall rebound tenderness Peritoneal inflammation

sign

Carnett's sign Loss of abdominal tenderness when abdominal wall muscles are contracted Intra-abdominal source of abdominal pain

Chandelier sign Extreme lower abdominal and pelvic pain with movement of cervix Pelvic inflammatory disease

Charcot's sign Intermittent right upper abdominal pain, jaundice, and fever Choledocholithiasis

Claybrook sign Accentuation of breath and cardiac sounds through abdominal wall Ruptured abdominal viscus

Courvoisier's Palpable gallbladder in presence of painless jaundice Periampullary tumor

sign

Cruveilhier sign Varicose veins at umbilicus (caput medusae) Portal hypertension

Cullen's sign Periumbilical bruising Hemoperitoneum

Danforth sign Shoulder pain on inspiration Hemoperitoneum

Fothergill's sign Abdominal wall mass that does not cross midline and remains palpable when rectus contracted Rectus muscle hematomas

Grey Turner's Local areas of discoloration around umbilicus and flanks Acute hemorrhagic pancreatitis
sign

Iliopsoas sign Elevation and extension of leg against resistance creates pain Appendicitis with retrocecal abscess

Kehr's sign Left shoulder pain when supine and pressure placed on left upper abdomen Hemoperitoneum (especially from splenic
origin)

Mannkopf's Increased pulse when painful abdomen palpated Absent if malingering

sign

Murphy's sign Pain caused by inspiration while applying pressure to right upper abdomen Acute cholecystitis

Obturator sign Flexion and external rotation of right thigh while supine creates hypogastric pain Pelvic abscess or inflammatory mass in pelvis

Ransohoff sign Yellow discoloration of umbilical region Ruptured common bile duct

Rovsing's sign Pain at McBurney's point when compressing the left lower abdomen Acute appendicitis

Ten Horn sign Pain caused by gentle traction of right testicle Acute appendicitis
 Laboratory and imaging studies can be used to
further confirm the suspicions, reorder the
proposed differential diagnosis, or less commonly,
suggest unusual possibilities not yet considered
 Haemoglobin, White blood cell count with differential,
CRP, Electrolytes, creatinine, lipase, Total and direct
bilirubin, LFT’s, A/VBG – lactate/acid-base, Urinalysis,
Urine/serum human chorionic gonadotropin
 Plain films
 Free gas
 Volvulus
 Calcifications
 5% of appendicoliths,10% of gallstones, and 90% of renal
stones, pancreatic calcifications, abdominal aortic
aneurysms, visceral artery aneurysm, and atherosclerosis
in visceral vessels
 CT
 Appendicitis, diverticulitis
 small bowel obstruction/ileus
 acute intestinal ischemia
 USS
 Gallstones, gallbladder wall thickness, fluid around
the gallbladder, diameter of the extrahepatic and
intrahepatic bile ducts
 intraperitoneal fluid
 ovaries, adnexa, and uterus
 RIF Pain Differential diagnosis
 Appendicitis
 Mesenteric adenitis
 Diverticulitis
 Bowel ischaemia/infarction
 Tumour
 Ovarian pathology
 PID
 Mittelschmerz
 Endometriosis
 Ovarian/testicular torsion
 Ectopic
 Obstruction
 Volvulus
 Intussusception
 IBD
 AAA
 Renal pathology
 Biliary pathology
 Meckel's diverticulitis
 Psoas abscess
 Rectus sheath haematoma
 Hernia
 Obstruction of the lumen
 appendicolith, lymphoid hyperplasia, vegetable matter
or seeds, parasites, neoplasm
 perforation typically occurs after at least 48 hours
– abscess formation
 Rarely, free perforation of the appendix into the
peritoneal cavity - peritonitis and septic shock -
complicated by multiple intraperitoneal abscesses
 Bacteria
 Escherichia coli, Streptococcus viridans, Bacteroides,
Pseudomonas
 History
 periumbilical pain
 followed by anorexia
and nausea
 pain localizes to RIF
 Fever and leukocytosis
 lethargy, irritability in
infants
 Occasionally - urinary
symptoms or
microscopic hematuria
 possible cause of small
bowel obstruction
(patients without prior
abdominal surgery)
 Examination
 look ill and are lying still
 Low-grade fever
 diminished bowel sounds
 focal tenderness (McBurney’s
point)
 In/voluntary guarding
 Percussion/rebound tenderness
 Dunphy's sign, Rovsing's sign,
obturator sign, iliopsoas sign
 If the appendix perforates,
abdominal pain becomes intense
and more diffuse, rigidity, HR
rises, T > 39°C
 Laboratory  Imaging
 WCC is elevated,  Ultrasonography sensitivity 85%,
75% neutrophils specificity 90% (operator dependent)
 WCC normal in 10%  Paeds and pregnant
 urinalysis excluding  >7mm diameter
pyelonephritis or  Target sign
nephrolithiasis  Appendicolith
 microscopic  CT sensitivity 90%, specificity 90%
hematuria is  >7 mm diameter
common in  circumferential wall thickening
appendicitis  halo or target
 fat stranding, oedema, peritoneal
fluid, phlegmon, abscess
 detects appendicoliths in about 50%
 CT most valuable among older
patients - diverticulitis and
malignancy
Treatment:
 resuscitation
 NBM
 IVF – aggressive if perforation suspected
 Antibiotics
 Analgesia
 antibiotics - aerobic and anaerobic colonic flora cover
 Non-perforated appendicitis - single preoperative dose of antibiotics
reduces postoperative wound infections and intra-abdominal abscess
formation
 perforated or gangrenous appendicitis, continue postoperative
intravenous antibiotics until the patient is afebrile
 Surgery
 Laparoscopy and laparoscopic appendicectomy
 Open appendicectomy
 Laparotomy
PC:
 60yo male presented to ED at 0800, seen by PHO
 Generalised abdominal pains eventually moving to right side since
night before, retching
PMX:
 Calf cramps, DVT, Carpal tunnel release x 2
O/E:
 Obs: HR 108, BP 166/79, RR 20, sat 97%, T 37.1 – SEPTIC (HR, RR,
WCC later)
 HS x 2, lungs clear
 RIF tenderness and rebound – “acute abdomen”
 Suspected Appendicitis, food poisoning, wanting to exclude
obstruction
 Bloods
 AXR
 USS
 Surg PHO contacted at 1330 (5.5 hours after arrival) with
diagnosis of appendicitis – SEPTIC
 WCC: 13.9
 Neutro: 11.55
 CRP: 19
 USS – appendicolith, appendicitis
 On surgical arrival therapy thus far:
 Obs: HR 80, BP 124/78, RR 18, sat 95%, T 37.8 – now febrile as well
 NBM
 Nil Fluids
 Nil Antibiotics

Laparoscopy Findings:
Acute appendicitis with purulent ascites
 Epigastric pain differential diagnosis
 pancreatitis
 Myocardial pathology
 Gastritis
 Oesophagitis
 Hiatus hernia
 Acute cholecystitis
 Biliary colic
 Biliary Obstruction
 Cholangitis
 Cholangiocarcinoma
 Pancreatic carcinoma
 Liver Abscess
 Hepatitis
 Diaphragmatic abscess
 Diverticulitis
 Appendicitis
 Duodenitis
 Bowel ischaemia/infarction
 Tumour
 Bowel obstruction
 Meckel's diverticulitis
 HCC
 Parenchymal and peripancreatic fat necrosis and
an associated inflammatory reaction
 Oedema, infiltration of inflammatory cells,
necrosis, thrombosis of intrapancreatic vessels,
vascular disruption, intraparenchymal
haemorrhage, intrapancreatic or peripancreatic
abscesses
 Causes
 70% to 80% - Abuse of ethanol or Biliary tract stones
 Drugs, ERCP, hypercalcaemia, hyperlipidaemia,
idiopathic, infections, ischaemia, parasites, post-
operative, trauma, scorpian sting
 History  Examination
 Abdominal pain
 Constant and
increasing
 Epigastric
 upper quadrants
 lower abdomen
 lower chest
 Knifelike, radiating
straight through mid-
central back
 nausea, vomiting
 rolling or moving around in search of a more
comfortable position
 ill and anxious appearance
 Temperature
 Hypovolemia
 Tachycardia
 Tachypnoea
 Hypotension
 collapsed neck veins
 dry skin
 dry mucous membranes
 diminished subcutaneous elasticity
 Diminished BS in lower lung fields
 Atelectasis, pleural effusion
 Some degree of jaundice
 Ileus – silent, distended, tympanitic
 Direct, percussion, and rebound abdominal
tenderness
 In/voluntary guarding
 flank ecchymoses (Grey Turner's sign) or
periumbilical ecchymoses (Cullen's sign)
 Laboratory  Imaging
 increased hematocrit,  Plain
hemoglobin, creatinine  Chest
 albumin depressed  Atelectasis
 hypochloremic metabolic  Effusion
alkalosis can develop  pneumonia
(vomiting)  Abdominal
 WCC usually elevated  Cut off
 Elevated CRP  ileus
 BSL may be elevated  CT
 Hyperbilirubinemia  it is generally believed that
 Hypocalcemia early contrast-enhanced CT
 disseminated intravascular does not worsen pancreatitis
coagulation
 thrombocytopenia,
prolonged aPTT, PT
 USS
 Elevated amylase/lipase  GB
 Cholelithiasis
 Severity Score >3  Treatment
 Aggressive fluid and electrolyte repletion is the
ADMISSION INITIAL 48 HOURS most important element in the initial
management of pancreatitis
 
Gallstone Pancreatitis
 Inadequate fluid resuscitation can worsen the severity
of an attack and lead to complications
Age > 70 yr Hct fall >10  Fluid management, although critical, may be
WBC >18,000/mm3 BUN elevation >2 mg/100 mL
particularly difficult when hypovolemia is combined
with the respiratory failure of ARDS
 Fluid balance required - IDC
Glucose > 220 mg/100 mL Ca <8 mg/100 mL
2+  nasogastric decompression may be needed
 Severe pancreatitis – IV meropenem
LDH >400 IU/L Base deficit >5 mEq/L  Feeding within 72 hours
AST >250U/100 mL Fluid sequestration >4 L
 parenteral nutrition
 NGT- small amounts nutrients
 
Non-gallstone
 Watch for cardiovascular collapse, respiratory
Pancreatitis failure, renal failure, metabolic encephalopathy,
gastrointestinal bleeding, disseminated
Age >55 yr Hct fall >10
intravascular coagulation
WBC >16,000/mm3 BUN elevation >5 mg/100 mL  intubation and respiratory support may be
required
Glucose >200 mg/100 mL Ca2+ <8 mg/100 mL  hemodialysis may be required
 ERCP
LDH >350 IU/L Fluid sequestration >6 L  Cholecystectomy
 Rarely necrosectomy
AST >250U/100 mL Base deficit >4 mEq/L

  Pao2 <55 mm Hg
PC:
 86 yo male presented to ED 1905, seen by RMO
 RUQ pain, anorexia, vomiting, diaphoresis, SOB since 1400
PMHx:
 IHD and MI, infra renal AAA, HTN, hypercholesterolaemia, Gout,
Type II IDDM, left adrenalo/nephrectomy for RCC, renal impairment,
cholecystectomy (10yrs ago), malignant melanoma (face),
hemicolectomy for colorectal Ca
O/E:
 Obs: HR 92, BP 200/103, RR 24, sat 99%, no temperature until 2030
36.2 – SEPTIC (HR, RR, WCC later)
 HS dual, lungs clear, Abdomen tense, distended, very tender RUQ
 Suspected visceral perforation – “acute abdomen”
 Bloods
 C/AXR

 RMO (end of shift) handed over to Resident

Contacted surg PHO 2200 (3 hours after arrival) with diagnosis of pancreatitis
 WCC: 14.7
 Neutro: 12.74
 Lipase: 3810
 Calcium: 2.17 (N)
 On surgical arrival, therapy thus far:
 Obs: HR 100, BP 189/90, no new T measured, RR 24, sat 100% - worsening condition
 NBM
 Nil fluids
 Nil antibiotics – rare
 No BSL chart
 No O2 therapy
 No IDC
 (NGT occasionally required)

Findings:
Severe pancreatitis secondary to choledocholithiasis
ICU admission
 RUQ pain differential diagnosis
 Acute cholecystitis
 Biliary colic
 Biliary Obstruction
 Cholangitis
 pancreatitis
 Cholangiocarcinoma
 Pancreatic carcinoma
 HCC
 Liver Abscess
 Hepatitis
 Diaphragmatic abscess
 Diverticulitis
 Appendicitis
 Duodenitis
 Bowel ischaemia/infarction
 Tumour
 Bowel obstruction
 Intussusception
 IBD
 Renal pathology
 Meckel's diverticulitis
 Symptoms attributable to biliary tract pathology
are usually the result of obstruction, infection, or
both. Obstruction can be extramural (e.g.,
pancreatic cancer), intramural
(cholangiocarcinoma), or intraluminal
(choledocholithiasis)
 History  Examination
 Pain  positive Murphy's sign
 constant pain  pain of acute cholecystitis is
 builds in intensity exacerbated by touch
 radiates to the back,  Scleral/cutaneous icterus
interscapular region,
right shoulder
 band-like tightness of
the upper abdomen
 Association with meals
Consider ascending
present 50% of patients
cholangitis
 Nausea, vomiting
 Jaundice
 Fever
 Laboratory  Imaging
 Inc WCC  Plain
 Inc CRP  15% of gallstones radiopaque
 Deranged LFT’s  Exclude FG and pneumonia
 Obstruction associated with  USS (operator dependent)
liver dysfunction and acute  high specificity (>98%) and
cellular injury sensitivity (>95%)
 Obstruction (Pathopneumonic)  GS and impaction
 Inc Bilirubin and ALP  GB wall
 Lipase  CBD dilation
 Pericholecystic fluid
 CT
 sensitivity about 55%
 Not as good for GB/GS
 Exclude other pathology
 Identify gangrenous GB

(MRCP/cholangiography
unavailable)
 Treatment
 Resuscitation
 IV fluids
 Analgesia
 Narcotic’s can cause spasm of Sphincter of Oddi
 IV Antibiotics – cover GNR, GPC, anaerobes
 Enterobacteriaceae (68% incidence) -  Escherichia coli, Klebsiella,
Enterobacter
 Enterococcus species (14% incidence)  
 Anaerobes (10% incidence) - Bacteroides species
 ERCP
 Cholecystectomy and IOC
 Open
 Laparoscopic
PC:
 72 yo male presented to MBH at 0530
 Febrile, Severe constant abdominal pain, nausea - Acute Abdomen
 Contacted surg PHO at 1400 (8.5 hours after presentation) for T/F with ?acute cholecystitis for USS
- accepted
 transferred from MBH ED at 2010 (14.5 hours after presentation)
PMHx:
 IDDM
 Colorectal Ca – APR and colostomy
 HTN – on beta blocker!
 CRI
 PVD – bilateral BKA
 Appendicectomy
O/E:
 Obs – HR 76, BP 108/51, RR 18, sat 90%, T 37.0
 No examination notes in HBH file
 Bloods (MBH)
 K 5.1, Ur 19.4, Cr 220, Glu 8.4, CRP 60, WCC 12.4, Neutro 10.44, Hb 91, LFT’s - OK
 USS arranged 2100
 ED SMO contacted Surg PHO at 2115 (in OT with consultant until 2400 – acute cholecystitis and
gangrenous cholecystitis) – 15.5 hours after presentation, with acute cholecystitis - SEPTIC
 USS
 Multiple GS
 Thickened oedematous GB wall
 Dilated CBD – 8.5mm
 Acute cholecystitis
 On surgical arrival (2400 – almost 4 hours since T/F, 18.5
hours after presentation), therapy thus far
 Hypotensive – BP 96/54, HR 72 (beta-blocked)
 IDC in-situ – no urine measures
 NBM
 No IV fluids at all (all day!)
 No analgesia since arriving in HBH – no fluid or medication chart
at HBH
 No insulin (IDDM)
 No BSL’s
 No repeat bloods
 Single dose of antibiotics at MBH prior to transfer

Findings:
Severely septic insulin dependent diabetic, chronic renal impaired
patient with acute cholecystitis
T/F to RBH ICU under general surgical team
 R/LIF pain differential diagnosis
 Diverticulitis
 Appendicitis
 Bowel ischaemia/infarction
 Tumour
 Obstruction
 Volvulus
 Intussusception
 IBD
 AAA
 Renal pathology
 Biliary pathology
 Meckel's diverticulitis
 Psoas abscess
 Rectus sheath haematoma
 Ovarian pathology
 PID
 Mittelschmerz
 Ovarian/testicular torsion
 Endometriosis
 Ectopic
 Hernia
 intestinal mucosal herniations through intestinal wall via natural
openings created by nutrient vessels in colonic wall -
pseudodiverticulum
 one or more become inflamed – unclear process
 obstruction, distension, overgrowth, vascular compromise, perforation
 wall erosion from increase pressure or particles, necrosis, perforation
 Micro-perforation – contained within pericolic fat/mesentery
 larger perforations can lead to:
 phlegmon/abscess formation
 intestinal rupture
 intestinal obstruction
 peritonitis
 fistula formation
 skin, bladder, vagina, small bowel
 haemorrhage
 History  Examination
 Abdominal pain  Septic
 LIF usually, cramping,  Tenderness
radiation  usually localised LIF (sigmoid
suprapubic/groin/back 50%, descending 40%, entire 5-
 altered bowel habit 10%)
 diarrhoea/constipation  generalised abdominal pain,
epigastric, RIF
 flatulence  peritonism – rebound,
 bloating guarding, rigidity, percussion
pain
 Fevers, sweats, chills,  Distended, tympanic
shakes  Mass
 Nausea, vomiting  phlegmon
 urinary symptoms –  abscess
pneumaturia, faecaluria  Fistula
 Reduced BS
 Laboratory  Imaging
 Bloods  Erect CXR
 FBC  free gas, other pathology
 eLFT’s  CT abdomen
 CRP
 pericolic fat stranding due to
 ABG inflammation
 Lipase  colonic diverticula
 BC
 bowel wall thickening
 Urine  soft tissue inflammatory
 dipstick, M/C/S, BHCG masses, phlegmon, abscesses
 Staging
 Uncomplicated or complicated
 Clinical staging by Hinchey's
classification is geared toward
choosing the proper surgical
procedure when diverticulitis is
complicated, as follows:
 Stage I disease - Small or
confined pericolic or mesenteric
abscess
 Stage II disease - Large abscess,
often confined to the pelvis
 Stage III disease - Perforated
diverticulitis causing
generalized purulent peritonitis
 Stage IV disease - Rupture of
diverticula into the peritoneal
cavity with faecal
contamination causing
generalized faecal peritonitis
 Treatment
 Resuscitation
 IV fluids and monitoring
 PO/IV antibiotics
 Analgesia
 Surgery when:
 Free-air perforation with faecal
peritonitis
 Suppurative peritonitis secondary to a
ruptured abscess
 Uncontrolled sepsis
 Abdominal or pelvic abscess
 USS/CT-guided aspiration if possible,
transanal vs transabdo (stage II)
 Elective resection after recovery if
drainage successful

Fistula formation
 Intestinal obstruction
 Failing medical therapy
 Immunocompromised status
 Recurrent episodes of acute
diverticulitis
PC:
 76 yo male presents to ED at 1957, seen by SMO
 2/52 abdominal pains worsening
PMHx:
 IHD – MI
 COAD
O/E:
 Obs – HR 132, BP 154/74, RR 28, sat 99%, T 38.7- SEPTIC
(T, HR, RR, WCC)
 HS x2, chest clear
 No findings charted “Acute abdomen”
 Bloods
 BC
 Urine dipstick
 CXR
 ED SMO contacted surg PHO at 2030:
 Acute abdomen – perforated diverticulitis
 bloods
 WCC 15.6
 CRP 168
 Urine
 Moderate blood
 CXR – free gas
 On surg PHO arrival 2100 therapy thus far
 2 x IVC
 500ml n/saline bolus charted but not yet begun
 Triple antibiotics charted but not yet begun
 No analgesia given
 No IDC

Laparotomy Findings:
Contained perforated diverticulitis with purulent peritonitis – spent 7 days in
ICU, 33 days in hospital
 What you want – advise, review, admission
 Name and age of patient
 Differential Diagnosis
 Other relevant history
 Clarify acceptance of admission
 If they require more detailed information they will
ask you
 Acute Abdomen
 After history, examination completed
 Differential diagnosis formed
 Investigations sent/ordered
 Resuscitation organised and begun
 Unstable surgical patient
 On arrival
 Multi-trauma patient
 Before arrival
 Stable surgical patient
 After history, examination completed
 Differential diagnosis formed and Investigations
performed to identify pathology (if within reasonable
time frame)