Abdominal Pain for Medical Finals (based on Newcastle university learning outcomes)

8/14/2019 Abdominal Pain for Medical Finals (based on Newcastle university learning outcomes)

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Hospital based practice Abdominal pain.

History.o First priority is to determine whether it is an acute abdomen requiring admission.o History should focus on pain, and then other symptoms.o For pain use usual SOCRATES questions.

Site.Site of pain CauseEpigastric Lower oesophagus.

Oesophagitis Malignancy Perforation

Stomach. Peptic ulcer Gastritis

Pancreas Pancreatitis Malignancy

Inferior MI

Righthypochondrium

Biliary tree Bilary colic Cholecystits Cholangitis

Liver Hepatitis Malignancy Abscess Right ventricular

failureSubphrenic space

AbscessLower lobe pneumonia

Lefthypochondrium

Spleen Traumatic rupture. Infarction

(associated withsickle cell disease)

Pancreas Pancreatitis Malignancy

Subphrenic space Abscess

Lower lobe pneumonia

Site of pain CauseCentral Pancreas

Pancreatitis Malignancy

Small/ large bowel. Obstruction Perforation Intussusception Ischemia

Inflammatory boweldisease Irritable bowel

disease Lymphoma Adhesions Early appendicitis

Lymph nodes Mesenteric adenitis Lymphoma

Abdominal aorta. Ruptured AAA

Right iliac fossa Terminal illeum. Crohns disease Infection (eg. TB) Meckels

diverticulumAppendix

Appendicitis Tumour (including

carcinoid)Caecum/ ascending colon.

Diverticulitis Paracolic abscess Ulcerative colitis Malignancy

Ovary/ fallopian tube. Malignancy Ectopic pregnancy Pelvic inflammatory

disease Bleeding cyst


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Torsioned cyst.

Site of pain CauseLeft iliac fossa Sigmoid/ descending colon.

Diverticulitis

Paracolic abscess Ulcerative colitis Malignancy

Ovary/ fallopian tube. Malignancy Ectopic pregnancy Pelvic inflammatory

disease Bleeding cyst Torsioned cyst.

Suprapubic Bladder.

UTI Acute urinary

retentionUterus/ adnexae

Pelvic inflammatorydisease

Endometriosis

Loin Kidneys Malignancy Pyelonephritis Polycystic disease

Ureters Stone Clot

Lower lobe pneumonia

Other causes of abdominal pain

Anxiety Vasculitis DKA Addisons disease Sickle cell crisis Lead poisoning Porphyria Familial

Mediterranean fever


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Onset

Sudden onset severe pains suggesto Perforationo Rupture of aorta

Colicky pain is due to spasm of:o Bowelo Ureterso Gall bladder o Against obstruction such as:

StoneTumour Foreign bodyStricturesStrangulated herniasIntussusception.

Gradual onset with sustained pain.o Inflammatory conditions

Inflammatory bowel diseaseInfectionAbscessGastroenteritisMalignancy

Radiation may help to suggest the origin. To back.

o Aortico Pancreatic

To shoulder tip.o Sub diaphragmatic pathology causing diaphragmatic

irritation. Ureteric pain

o Loin to groin.

Exacerbating and relieving factors. Peritoneal irritation made worse by movement. Colicky patients may draw knees up and roll around.


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o Associated symptoms.Vomiting is common

Projectile vomiting is a sign of pyloric stenosis Faeculent vomiting is a sign of large bowel obstruction.

Haematemesis. Upper GI bleeding.

Rigors. Suggest sepsis.

o Abscesso Cholangitiso UTIo Gram ve septicaemia

Changes in bowel habit. May be an important symptom. Absolute constipation indicates obstruction. Diarrhoea.

o Gastroenteritiso Diverticulitis

Alternating constipation and diarrhoea.o Colonic malignancyo Irritbale bowel syndrome

Rectal bleeding. Malignancy Inflammatory bowel disease Diverticulitis Dysentry Angiodysplasia Dark red bleeding suggests bowel infarction.

Features of UTI. Dysuria Haematuria Increased urinary frequency

Vaginal discharge will often occur with pelvic inflammatory disease.

o Other factors.Past surgical history.

AdhesionsPast medical history.

Known AAAPrevious occurrences.

Recurrent UTIFamily history.

Eg. porphyria


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Drug history. Opiates causing constipation.

Examination.o First question is to assess if patient is critically ill.

Shock Tacchycardia Hypotension Increased Capillary refill time.

o Except in septic shock.

Reduced urine output Consider

o Septicaemia.Particularly Gram negative

o Severe bleeding.Ruptured AAARuptured spleen

o Fluid loss.ComitingDiarrhoeaPancreatitsThird spacing in bowel obstruction

o Acute Addisonian crisis.

Peritonism. Guarding Distension Absent bowel sounds

o Parlysis of peristalsis Rebound tenderness

Causes.o Infections.

Spread from paracolic/ subphrenic abscessFollowing surgery or paracentesisBowel perforation

o Chemical irritation.BileFaecesGastric acidPancreatic enzymes

o Transmural inflammation


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Crohns diseaseSalpingitis.

o Examination can suggest the underlying cause.Pyrexia.

High grade suggests infection. Low grade suggests.

o Malignancyo Bowel infarctiono Inflammatory bowel diseaseo Pancreatitis.

Jaundice. Hepatitis Pancreatitis

Dehydration. Rapid fluid loss

Cachexia. Chronic pathology Particularly malignancy.

Clubbing. Inflammatory bowel disease.

Blood pressure Shock

Hands: Clubbing,Anaemia

Abdomen:Surgical scar,Distension, Bruising,Tenderness, Guarding,Mass, Ascites,Bowel sounds.

Uroigenital:Hernial orifices,Rectal examination,Vaginal exam,Pregnancy test,

Urine dipstix.

Pulse: Tachycardia

General: Unwell, Pyrexia,Dehydration, Jaundice,Cachexia, Lymphadenopathy.


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Small bowel lymphoma Chronic liver disease.

Lymphadenopathy. Lymphoma Metasteses.

o Virchows node in CA stomach.Abdominal bruising.

Pancreatitis Leaking aortic aneurysm Cullens sign

o Periumbilical Grey Turners sign.

o FlanksRecent surgical scar.

May indicate source of peritoneal sepsis. Eg. anastomotic leak.

Older surgical scar. May suggest presence of adhesions.

Distension. If marked.

o Indicates bowel obstruction.o Accompanied by resonant percussion note.o Occasionally peristalsis may be visible.

Peritonitis may cause distension.Tenderness.

Important to consider the structures that are below the site of tenderness.

Peritonism indicated by:o Rebound tendernesso Guarding

Mass. Neoplastic. Inflammatory

Ascites. Malignancy Peritoneal sepsis Pancreatitis Portal hypertension.

Bowel sounds. High pitched (tinkling).

o Obstruction Absent.

o Paralytic illeus.Hernial orifices.

Inguinal Femoral Check particularly carefully in suspected obstruction.

Pelvic and rectal examination. Pelvic inflammatory disease Cervical excitation


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Ectopic pregnancy Rectal mass Rectal bleeding Stool consistency.

Urine dipstix. White cells.

o Infection Red cells.

o Stoneo Tumour o Infection

Glucose Ketones

Cardiorespiratory exam. Myocardial infarction Basla pneumonia

Investigations.o All patients admitted should have FBC and serum biochemistry performed.o Further tests depend on differential diagnoses.


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o FBC.Leucocytosis is seen in:

Infection Inflammation Malignancy

Anaemia seen in: Acute blood loss Chronic pathology Malignancy

o Serum amylase.Very high in acute pancreatitis.May also be raised in:

Abdominal Pain

HistoryExamination

MSUSimple haematologySimple Biochemisty

Sudden onsetSevere ain

Colicky pain Gradual onsetSustained ain

Atypical pain withnormal investi ations

Perforation or ruptured bowel

AneurysmSpleen

Pancreatitis

Bowel obstructionStrangulated hernia

GallstonesRenal stones

Irritable bowelsyndrome

AbscessMalignancy

Inflammatory boweldisease

Consider:Anxiety

Munchausenssyndrome

Unusual causes.

Urgent admissionFBCU&ECa2+

GlucoseLFTs

Amylase

AXR US Scan

Erect CXR

Consider:

US scanCT scan

ColonoscopyEndoscopy

Small bowel enema

Sudden onsetSevere pain


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Perforated peptic ulcer DKA Cholecystitis Abdominal trauma MI

o U&Es.DehydrationRenal failureDue to:

Obstructive uropathy Shock.

o Serum calcium.Hypercalcaemia seen in:

Renal stones Pancreatitis.

Hypocalcaemia seen in. Pancreatitis.

o Blood glucose.Hypoglycaemia will result from.

Liver failure Addisons disease.

Hyperglycaemia will be present in: Ketoacidosis Complicated acute pancreatitis.

o LFTs.Abnormal in:

Acute hepatitis Bilary disease Shock.

o MC&S of MSU.Exclude infection.

o AXR.Only acutely indicated in suspected

Bowel obstruction Renal stones Pyelonephritis.

o Abdominal ultrasound.Dilatation of

Bilary tree Ureters

Intra abdominal massAscitesAbscess.


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Acute Renal failure.

Presentation.o Normally present whilst and inpatient with.

Elevated creatinine and urea.Oliguria.

o Sometimes present to A&E with.MalaiseConfusionSeizuresComa

Nausea & VomitingAnorexiaOliguria or abnormal urine colour Haematuria.

Pink, rather than frank bloodDrug overdose.

Eg. paracetamol

Constitutional symptoms. Arhtralgia Rhinitis Respiratory symptoms

Vasculitic rashMulti organ failure

o In the majority of cases, failure can be resolved with:Adequate volume replacementTreatment of sepsisStopping nephrotoxic drugs

Assessment of severity.o Is there life threatening hyperkalaemia or pulmonary oedema?o Determine the cause.o Is the patient still passing urine?

Does it look normal?o ECGo Urgent U&E and ABGso CXR

o Pre renal causes.Account for 75% of cases.Check postural BP and HR

Assess volume status. Check CVPSepsis screen

o Renal causes.Account for 20% of cases.Urinalysis and microscopy.

For blood/ castsDrug historyCPK/ myoglobin in urine.


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o Post renal causes.May have anuria.

o Acute renal failure has a mortality of about 50%o The following history can be important.

History of fluid loss. D&V Diuretics Bleeding Fever Diarrhoea may suggest:

o Haemolytic uraemic syndromeo Hypovolaemia

History of sepsis. UTI Fever or hypothermia Bacterial endocarditis Non specific illness in the elderly.

Drug history. NSAIDs ACE inhibitors Aminoglycosides Amphotericin Anti HIV drugs

Non specific symptoms. May suggest vasculitis

o Myalgiao Arthralgiao Neurological signso Ophthalmic complicationso Sinusitiso Skin rashes

Past history of. Hypertension Diabetes

o Increased risk of contrast induced renal impairment.o Dont allow to become dehydrated.

Renovascular disease Prostatism Haematuria

Signs & symptoms of liver disease.

Back ache. May suggest pelvi ureteric obstruction. May originally affect a single kidney Likely to develop in both kidneys Consider AAA

Cholesterol emboli. Aneurysms Absent pulses


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RashPost partum.

HELLP syndrome HUS Fatty liver disease Pre - eclampsia

Look for signs of fluid overload. Dyspnoeic with signs of pulmonary oedema High JVP High CVP Peripheral oedema Gallop rhythm

Look for signs of dehydration. Postural hypotension Reduced tissue turgor.

o Poor prognostic features include.Age > 50 yearsInfection.

Especially septicaemiaBurns.

> 70% body surface area.Rising urea.

> 16 mmol/24 hoursOliguric for > 2 weeksMulti organ failure.

> 3Jaundice

o Main priority is toStabilise patientTry and prevent cardiovascular collape.

Causes.o Pre renal.

HypovolaemiaHypotension/ Shock Renal artery emboliRenal artery stenosis, with ACE inhibitor therapyHepatorenal syndrome

o

Renal. Vasculitis SLE PAN

Glomerular nephritisAcute tubular necrosis

Ischemia (eg. hypotension) Septicaemia Toxins.


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o Myoglobino BJ protien

Drugs.o Gentamicino Contrast

Prolonged pre renal oliguria Malaria

Thrombotic microangiopathy Accelerated hypertension Thrombotic thrombocytopaenic purpura Haemolytic uraemic syndrome.

Sclerodermic crisisSepsis

Interstital nephritis Drugs

o NSAIDSo Antibiotics

Infections. Staph Strep Leptospirosis Brucella G ve sepsis Legionella

Crystalising ion overload. Calcium Urate Oxalate

Tumour lysis syndrome.o Post renal.

Renal vein thrombosisIncreased intra abdominal pressureHIV drugs.

Indinavir Intrabular pathology.

Uric acid crystalsUreteric

Stones Retroperitoneal fibrosis/ tumou

Urethra Prostatic hypertrophy.

o Causes of immune mediated ARF and vasculitis.Microscopic polyangitisWegeners granulomatosisChurg Strauss syndromePolyarteritis nodosaSLERA.

Disease & treatment


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Goodpastures syndromeCryoglobulinaemiaHenloch Schonlein purpuraAcute proliferative glomerulonephritisAcute interstitial nephritisHIV

MyelomaLeptospirosis

Interstitial nephritisHanta virus

Pulmonary renal syndromeInfective endocarditisIgA nephropathy.Drugs.

Penicillamine Amphetamine.

Investigations.o Urgent investigations in suspected ARF.

U&EsFBC & Blood filmCoagulation studies.

PT APTT TT Fibrinogen FCPs.

CPK HaptoglobinBlood culturesUrine MC&S

Urine sodium & osmolalityUrinary myoglobulinECGCXR US kidneys.

Size of kidneys Obstruction

Consider other investigations to aid diagnosis.

o U&Es.Urea is disproportionately raised in

Pre renal failure. Uraemia GI bleeds Catabolic states.

o Calcium & Phosphate.Acidaemia increases ionised calcium

o FBCAnaemia suggests.

Chronic renal failure Acute on chronic failure


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Low platelets suggests Liver disease HELLP Sepsis

Increased platelets suggest. Vasculitis Eosiniphilia Churg Strauss syndrome Interstitial nephritis

o CoagulationAbnormal in.

DIC Liver disease SLE HELLP syndrome HUS

o LFTs.Acute hepatitisParacetamol overdoseCirrhosisALP often increased in vasculitis

o LDH/HBD.Increased in HUS

o CPK.

Very high in rhabdomyolisiso Blood cultures.

Should be taken from all patients with ARFo Immunology.

ANCAAnti GBMImmunoglobulin levelsC3/C4Rh factor ANAENAdsDNACryoglobulinsAntiphopholipid antibodies.

Anti cardiolipin

Anti 2 glycoprotein.o ESR/CRP.

CRP often normalESR raised in SLE

o Protein strip.For prarprotiens.

Myeloma Light chain disease

o Serology for dialysis.


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HIVHBsAgHCVAb

o Urine.Inspect urine yourself.

Contact renal reg on call or microbiology technician for urgent microscopy.Save urine for

Cytology if haematuria is main symptom. Bence Jones protein if myeloma suspected.

RBC casts suggest glomerulonephrits. Refer urgently to renal physicians.

Pigment casts suggest myoglobinuria.WBC casts suggest acute pyelonephritisExcess eosinophiluria associated with interstitial nephritis.Urine electrolytes and osmolality.

May help. Should not replace careful history and examination. Unreliable when diuretics have been taken. May be less reliable in the elderly with sub clinical renal impairment.

Pre - renal Renal

Urine sodium (mmol/L) < 10 > 40Urine/ serum creatinine > 40 < 20Urine osmolality > 500 < 350Urine/serum osmolality > 1.2 < 1.2

o US scan.

All patients with ARF should have urgent US scan to. Exclude obstruction Assess kidney size.

o Small in acute on chronic failure. Assess blood flow on Doppler imaging.

o CXR.Heart size.

Dilated in pericardial effusionPulmonary vasculature.

Pulmonary oedema Kerley lines.

Lung fields.

fluffy shadows Oedema Haemorrhage.

o Wegnerso Goodpasturess

Infectiono ECG.

Hyperkalaemia. Tented T waves


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Broad QRSSigns of myocardial ischaemiaSigns of pericarditis.

Management.o Fluid balance.

Manage on ITU or HDU.Measure

Weight BP.

o Supineo Standing

Pulse rateAssess hydration

Central skin turgor Mucous membranes JVP

Insert Central venous line. Measure CVP

Monitor PCWP in patients who are: Hypoxic Severely compromised.

Examine: Fluid charts Weight charts Operation notes.

If volume depleted. Give trial volume expansion of 500 ml 0.9% saline or colloid over 30

minutes if:o Low or normal CVPo Postural hypotension.

o Monitor response of urine output and venous pressure.o Continue until CVP = 5 10 cm at mid clavicular line.

When adequately filled (CVP > 10 cm and/or PCWP > 15 cm) reassessurine output.

If oliguric or anuric give:o Frusemide 120 250 mg IV at maximum of 4 mg/minute.o Frusemide infusion of 5 10 mg/hour.

If hypotension persists (MAP < 60 mmHg), commence inotropicsupport as for shock.

If fluid overloaded.. Consider urgent haemofiltration or dialysis.

o Indications.Persistant [K] > 7 mmol/LRefractory pulmonary oedemaPericarditis.

Heralds risk of tamponadeAcidosis.

pH < 7.1


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Bicarbonate < 12 mmol/LSymptomatic uraemia.

Tremor Cognitive impairment Coma Fits Urea > 45 mmol/L

o Consider venesection if there is a delay for dialysis.o Remove 250 500 ml.

Give oxygen to maintain SaO 2 > 95%.o Consider CPAP

Start IV nitrates.o Eg. GTN 2 10 mg/h

Give frusemide.o 120 500 mg IVo 5 10 mg/h infusion

Paracentesis, if tense ascites present. Avoid opiates.

o Single dose of 2.5 mg diamorphine may help relieve anxietyand sensation of breathlessness.

o Hyperkalaemia.In general terms, absolute potassium value is less important than the effect onheart muscle (Tented T waves, Broad QRS, flattened P waves).

If K > 7 mmol/L, treat urgently. If hyperkalaemia is unexpected finding, and ECG is normal, urgently

repeat blood potassium.

If K > 7 mmol/L or ECG shows hyperkalaemic changes, contact renal team andarrange for urgent dialysis if appropriate.While this is being set up.

Record 12 lead ECG and set up continuous cardiac monitoring. Give 10 ml of 10% calcium gluconate IV.

o Repeat every 10 20 minutes until ECG normalises.May require up to 50 ml.

o IV calcium doesnt reduce potassium levels, but reducescardiac excitility.

Give nebulised salbutamol (5 10 mg) to drive potassium into cells.o Use lower doses in patients with IHD.

Give 50 ml of 50% dextrose with 10 units of Actripid insulin over 15 30 minutes.

o Should lower [K] for several hours.


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Give 50 100 ml 8.4% sodium bicarbonate via central line over 30minutes.

o Or 400 ml 2.1% peripherally.o Represents sodium load of 50 100 mmol.

Give 250 mg frusemide of 5 mg bumetanide IV over 1 hour. Give polystyrene sulphonate resin enema (calcium resonium) 30g.

o Increases gut losses of potassium.o Follow up with 15 g PO TDS with regular lactulose.o Takes 24 hours to have an effect.

Monitor serum potassium frequently to assess response to treatment.

Further management.o Correct other abnormalities.

Acidaemia. Presentation

o Kussmauls breathingo Worsened hypotension

If pH < 7.2 give 100 ml 8.4% sodium bicarbonate through central line.o Or 400 ml 2.1% sodium bicarbonate via peripheral line.

Arrange urgent dialysis. Correction can cause symptomatic hypocalcaemia.

Hyponatraemia. Usually dilutional due to relative water excess. Manage as with other cuases of hyponatraemia.

Hyperphosphataemia. If [Ca]x[PO 4] > 4.6, risk of metastatic precipitation is high. Aim to lower [PO 4] to 0.6 1.4 mmol/L.

o Give oral phosphate binders.o Eg. Calcium carbonate 300 1200 mg TDS

Phosphate normally falls with dialysis or haemofiltration. New drug, Sevalmer at 806 mg TDS will lower [PO 4].

Nutrition. No role for protein restriction. Institute entral or parentral feeding early. In diabetics, insulin requirements fall with renal impairment.

Sepsis. Common precipitant/ complication of ARF. Culture all potential infection sites and fluids. Treat with appropriate antibiotics.

o Remember to adjust dose due to renal impairment.

Anuria.o Causes.

Obstructed urinary tract. Bilateral ureteric obstruction Bladder outflow obstruction.

Renal infarction.


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Prolonged hypotension in patients with atherosclerosis of renal arteries.Acute renal failure.

o Assessment.History and examination

Prostatism Haematuria Back ache ACE inhibitors Recent antibiotics NSAIDs Recent renal angioplasty Recent angioplasty Constitutional symptoms of glomerulonephritis History of loss of kidney.

Dangerous HyperkalaemiaECGUrgent U&EsABGsCXR.AXR

o Management.As for ARF.If bladder or pelvis mass large and palpable.

Insert catheter to exclude retention.If bladder is empty.

Urgent US to exclude bilateral ureteric obstruction or obstruction of single functioning kidney.

Determine level of obstruction with antegrade imaging. Treat bilateral hydronephritis with nephrostomies.

If US is negative, arrange urgent CT of abdomen.If obstruction is absent.

Cant exclude acute obstruction on US. Isotope renogram to determine renal perfusion.

o Absent renal perfusion suggests infarction. Retrograde uretrogram to look for obstruction.

Upper GI Bleeding.

Presentation Haematemesis.

o

Bright redo Dark clotso Coffee grounds

Malaena.o Signs.

Black StickySmelly

o Can arise from anywhere up to the caecum


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o Blood is cathartic and takes 4 6 days to be passedo With massive bleeding (eg. variceal) there may be dark clots in the stool.o Other causes of dark stool include:

Iron therapyBismuthLiquorice

Red wineGuinness

Weakness Sweating Palpatations Postural dizziness and fainting Collapse or shock.

Causes. Peptic ulcer 35 50% Gastroduodenal erosions 8 15% Oesophagitis 5 15% Varices 5 10% Mallory Weiss tear 15% Vascular malformations 5% Rare miscellaneous 5%

o Meckleso Crohns

Upper GI malignancy 1%

Assessment of severity. Important to categorise patients on admission into high or low risk of death. Most deaths are in elderly patients with co morbidities.

Rockall ScoreVariable Points scored

0 1 2 3Age (years) < 60 60 79 > 80Shock None HR > 100

SBP > 100HR > 100SBP < 100

Co morbidity Nil Cardiac Liver


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RenalMalignancy

Diagnosis Mallory Weisstear

All Other GI tractmalignancy

Stigmata of recent bleeding

None or dark spot Blood in upper GItract.

Adherent clot.Spurter Score < 3 = excellent prognosis Score > 8 = High risk of death

In general, things conferring a high risk of death are:o Age > 60 years.

30% risk of death if > 90 years.o Shock.

SBP < 100 mmHg in patients < 60 years.SBP < 120 mmHg in patients > 60 years.Measure postural changes in non shocked patients.Monitor heart rate.

o Chronic liver diseaseo Other chronic disease.

CardiacRespiratoryRenal

o Bleeding diathesiso Decreased GCS.

Management. Liaise early with specialists.

o On call endoscopyo Surgeons

Experienced anaesthetist should be informed. Most patients will have stopped bleeding by the time they are seen.

o All upper GI bleeds should be taken seriously.o May re bleed in hospital.o Mortality following re bleed is high.


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Priorities are.1. Stabilize patient2. Identify source of bleeding3. Definitive treatment of cause to stop the bleeding.

Stabilize patient.o Protect airway

Position patient on their sideo Restore circulating volume

Two 14 16G cannulae for fluid resuscitation. If peripheral veins are difficult, try:

o Jugular o Subclaviano Femoral

CVP monitoring allows early identification of bleeding. Useful to prevent over filling. Essential in the elderly or those with massive haemorrhage.

Fall of 5 cm H 2O over 2 hours suggests re bleed.If no signs of haemodynamic compromise.

1 litre 0.9% saline over 24 hours. Maintains patency of line.

Check for signs of low intravascular volume. Tachycardia Hypotension Postural fall in BP Postural increase in HR by > 30 bpm.

If low intravascular volume. 500 ml 1 L colloid over 1 hour. Crystaloid until blood is available. Stable BP takes priority over body sodium balance.

Use compatible blood when available. 1 unit/hour Until volume restored or CVP = 5 10 cm. If rate of bleeding is slow give packed cells. If massive haemorrhage, give O ve blood. Take G&S before blood is given for retrospective cross matching.

Monitor urine output. Catheterize patient if signs of haemodynamic compromise. Aim for >30 ml/h Prompt resuscitation should restore normal urine output.

Watch for signs of overload. Raised JVP Raised CVP Pulmonary oedema Peripheral oedema


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Too rapid transfusion can cause pulmonary oedema even before totalvolume lost has been replaced.

Identify cause of bleeding.o History.

Dyspepsia

Alcohol useDrug history.

NSAIDs Anti - coagulants

Risk factors for liver disease Normal vomit prior to haematemesis.

Mallory Weiss tear Variceal bleed

Previous GI bleeds Ulcers Surgery

o Physical examination.Stigmata of chronic liver disease.

Hepatomegaly Splenomegaly

Scars from previous surgeryTelangiectasia

Osler Weber Rendu syndromeAbdominal bruitsBruisesPR may reveal.

Malaena Semi fresh blood.

o Take bloods.FBC

Hb and PCV do not fall until plasma volume has been restored.


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If low at presentation, suggests massive bleed or acute on chronic picture.

WCC may be elevated.o Normally < 15 x 10 9/Lo If raised look for sepsis, which can predispose to

haemorrhage.

Platelets may be low in.o Hypersplenismo Chronic liver disease.

U&E. If urea is increased in proportion to creatinine, suggests protein

absorption in the gut.BM may be low in patients with chronic liver disease.If liver disease is suspected, take.

Clotting screening LFTs

Group and Cross match 4 8 units.Monitor ABG in severely ill patients.

o Consider passing NG tube.May help confirm coffee grounds or blood in stomach.Useful in diagnosing re bleedingHowever.

Blood easily Uncomfortable May predispose to

o Further bleedingo GORDo

Pulmonary aspirationDont put anything down tube, and keep patient nil by mouth, until endoscopyhas been performed.

o Upper GI endoscopy.Should be done within 12 hours of bleed.May be difficult to precisely locate site of bleeding due to clots in the stomach.Easy to exclude blood free sites.

May help to determine further management.Upper GI bleeding due to cirrhosis is non variceal in 30% of cases.After endoscopic treatment of bleeding ulcers, about 20% re bleed.Give IV Omeprazole or pantoprazole.

o Selective arteriography.If site of bleeding unable to be identified.

2 negative endoscopies.Bleeding is brisk.

0.5 1 ml/minSite to check include:

Superior mesenteric artery Inferior mesenteric artery.


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Coeliac axis.o Barium studies.

May be used to diagnose small bowel causes of malaena. Crohns Tumour

Labelled RBC scans may also be useful.Meckles scan may be useful in younger patients.

o Capsule endoscopy.Increasingly used in some centres.

General measures to stop the bleeding.o Correct any coagulopathy.

Platelet count < 50 x 10 9/L should be treated with platelet support. 6 12 units of platelets.

If patient is on anti coagulants. Assess need for anti coagulants before reversal.

o If patient may require re anti coagulantion (eg. prostheticmitral valve) correct with

Fresh frozen plasmaVery low dose Vitamin K (0.5 1 mg IV)

Otherwise, give.o 2 4 units fresh frozen plasmao IV Vitamin K 5 10 mg.

Cryoprecipitate may be required if fibrinogen levels are low.o Serum calcium may fall if several units of citrate containing blood is given.

Give 10 ml (4.5 mEq) calcium gluconate for every 3 4 units transfused.Supplement magnesium and phosphate as required.

Increased risk of being low in alcoholics.o Ulcer healing agents.

Give IV Proton pump inhibitor, either. Omeprazole 80 mg.

o Follow up with 8 mg/h for 72 hours. Pantoprazole 40 mg OD

Tranexamic acid. 0.5 1.5g TDS IV or PO. Increases levels of fibrinogen

DDAVP may be helpful in patients with renal failure.


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Peptic ulcer disease. Bleeding peptic ulcers form the mainstay of upper GI bleeds.

o

Account for 60% of bleedso A third of these have been taking NSAIDs.

Patients may have a history of:o Epigastric paino Relieved by food

Often there is no previous history.

Endoscopy allows the bleeding site to be visualised.o Identification of the vessel or an adherent clot has prognostic implications.

> 80% of these will re bleed.If no stigmata seen, < 5% will re bleed.

o Bleed may be treated endoscopically with.Electro coagulation.Heat coagulationLaser photo coagulation.Injection of adrenaline or alcoholInjection of endo clips.

o Keep patient Nil by Mouth for 6 8 hours post endoscopyIn case repeat endoscopy or surgery is required.

o Biopsy for H. pylori infection.If positive, start eradication therapy.

Surgery is indicated if:o Exsanguinating haemorrhage.

Bleeding too fast to replace.o Profuse bleeding.

> 6 units blood in initial resuscitation.Continued bleeding at > 1 unit in 8 hours.Persistant hypotension.

o Re bleed in hospitalo Failed endoscopic repair.o Re bleed following endoscopy in patients aged > 65 years.o Lesions at high risk of re bleeding.

Posterior DU with visible vesselsGiant gastric ulcer.

o Special situations.

Patients with rare blood groups.Patients refusing transfusions.

Medical management.o Treat with PPI for 4 8 weeks.o Repeat endoscopy at 6 8 weeks to check if lesion has healed.

Prognosis is good.o Overall mortality is < 10%


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o Mortality is reduced by early surgery in high risk patients.

Erosive gastritis/ oesophagitis. Generally present as relatively minor bleeds.

o May be significant. Account for 15% of upper GI bleeds. Present in.

o Previously well patients taking NSAIDs or Aspirin.o Critically ill patients who suffer an additional stress.

Managemento At endoscopy, there is normally a generalized ooze of blood from the inflamed mucosa.o Initial management is as with peptic ulcers.o Give PPI or sucralfate 1 2 g QDS PO or via NG tube.

PPIs are better than H 2 antagonists in healing oesophagitis or oesophagealulcers

o Correct any clotting disorders.o If lesions are diffuse and bleeding is continuing, partial gastric resection may be

necessary. Prognosis.

o 6% with haemorrhagic gastritis require surgery.o Overall mortality is < 10%.

Variceal haemorrhage. Oesophageal and gastric varices are caused by portal hypertension. Bleeding from varices is typically.

o Vigerous.o Difficult to control.o Occurring in the setting of:

Abnormal clottingThrombocytopaeniaSepsis.

Diagnosiso History and examination may riase suspicion of variceal source of bleeding.

30% of cirrhotics have a non variceal source of bleeding.o Most reliable diagnostic tool is upper GI endoscopy.

Perform as soon as feasible.o Bleeding may occur from.

Oesophageal varices.Gastric varices.Portal hypertension induced gastropathy.

Rare. Medical management.

o Resuscitate as for any bleeding.o Transfuse as necessary with.

Whole bloodFresh frozen plasma


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Plateletso Avoid over transfusion as may worsen situation.

Increases portal pressure.Increased risk of re bleeding.

o Give single dose of Vitamin K 10 mg IV.o Give bolus dose of Metoclopramide 20 mg IV.

Transiently decreased oesophageal pressure.Decreases azygous blood flow.

o Antibiotics.Take samples for MC&S.

Blood Urine Ascitic fluid

Start broad spectrum antibiotics. Variceal bleeding is associated with sepsis. Third generation cephalosporin. Ciprofloxacin and amoxicillin Treat for 5 days.

o Terlipressin (glypressin).2 mg initially.Follow with 1 2 mg every 4 6 hours for 72 hours.Causes splanchnic vasoconstriction.

Reduces variceal bleedingReduces mortality by 34%.Side effects.

Occur in 4%. Hypertension Skin ischaemia Splanchnic ischaemia

Nitrates ineffective in controlling peripheral side effects.Octreotide.

Synthetic analogue of somastatin No cardiac side effects. No need for nitrates Doesnt reduce mortality. 100 g IV bolus 25 50 g/h IV infusion.

o 500 g in 50 ml at 2.5 5 ml/h.Vasopressin.

Rarely used. Add 120 units to 250 ml 5% dextrose solution. Infuse 50 ml over 15 minutes.

o 24 units. Follow up with50 ml/h for 12 hours. Nitrates given to minimise cardiac side effects.

o Nitrates infusiono GTN transdermal patch.

o Endoscopic injection.


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Sclerosant into varices or para variceal region.Can control the acute bleeding.Side effects.

Are serious in 7% Immediately after injection.

o Retrosternal paino Fever

Mucosal ulceration Oesophageal strictures.

Emergency injection should be followed up. Repeat injection until varices are obliterated.

Gastric varices are more difficult to inject. Thrombin should be used.

o Band ligation.Frequently used.Technically more difficult in context of acute haemorrhage.

o Balloon tamponade.

Sengstaken Blakemore or Liton tube may be inserted.Inflation of gastric balloon only usually surfices.Remove within 12 hours due to risk of ischaemic ulceration.

Particularly if terlipressin is being co administered.o If liver failure present.

Give lactulose 10 15 ml TDS PO or via NG tube. Prevents encephalopathy.

Supplement as necessary with: Thiamine Multivitamins

For severe encephalopathy give enemas of: Magnesium Phosphate.

Radiological management.o TIPS is available in some centres.o Hepatic vessels are cannulated and stented to the portal system via.

Jugular veinFemoral vein.

o Allows portal system to be decompressed to 12 mmHg.

Surgical management.o Largely superseded by TIPS.o Emergency porto caval shunting.

95% effective in controlling bleed.Operative mortality of > 50%.Doesnt improve long term survivalVery few surgeons can do this procedure any more.

o Oesophageal transaction.Very rarely used in the UK.

Prognosis.o Overall mortality is 30%.


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o Mortality highest in those with severe liver disease.Grade C Child Pugh score

Points scored1 2 3

Encephalopathy grade None 1 2 3 4Ascites Absent Mild Moderate severe

Bilirubin (mol/L) < 35 36 60 > 60Albumin (g/L) > 35 28 35 < 28PT (seconds prolonged 1 4 4 6 > 6

Grade A < 6 Grade B = 7 9 Grade C > 10

o Success rate for stopping acute bleeding varicies depends on the technique.

Injection, sclerotherapy or banding 70 85%Balloon tamponade 80%Terlipressin 70%Octreotide 70%Vasopressin and nitrates 65%

Long term management.o Injection sclerotherapy.Weekly injections until variceal obliterated.

Normally about 1 month. Repeat at 3 6 month intervals.

Injection with 0.5 1 ml sclerosant in paravariceal region. 1 1.5 ml sclerosant into variceal.

o Banding ligation.Similar regimen to injection therapy.Achieves variceal obliteration in about a month rather than 2 months for injections.

o

Propanolol.80 mg TDSAim for 30 40% reduction in resting heart rate.Confirm reduction of portal pressure by measurement of hepatic venous wedge

pressure gradient.Reduces rate of re bleeding from varices and portal hypertensive gastropathy.

Not been shown to decrease mortality.o TIPS or shunt procedures

Provide more definitive cure.Re bleeds tend to occur only when shunt blocks.Increased incidence of chronic hepatic encephalopathy.

Mallory Weiss tear. Tear in the mucosa at gastro oesophageal junction. Follows severe retching. Particularly common following large bouts of alcohol consumption. Vomit normal initially, but becomes bright red.

Management.o Most stop bleeding spontaneously.o Tamponade with Sengstaken Blakemore tube may be used.


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o Surgical over sewing over bleeding point or selective arteriography and embolization of feeding artery may be necessary.

Cholelithiasis. Results from presence of gallstones in the gall bladder. Spectrum ranges from asymptomatic to full blown cholangitis.

Symptomatic cholelithiasis Intermittent post prandial epigastric/ RUQ pain.Due to transient cystic duct obstruction by stone.

No fever or raised WCCLFTs normal

Acute cholecystitis Acute gallbladder inflammationDue to cystic duct obstruction

Perisitent RUQ painFever may be presentWBC are raisedLFTs are raisedMurphys sign

Chronic cholecystitis Recurrent bouts of colic or acute cholecystitis.Leads to chronic gall bladder inflammation/ fibrosis

No fever Normal WCC

Acalculous cholecystitis Gall bladder inflammation due to bilary stasis.Only causes 5% of bilary disease.Occurs mainly in critically ill patients.

Choledocholiathiasis Gallstone in the common bile duct.

If primary disease, the stone originated thereIf secondary disease, stone originated in gall bladder and became wedged in the duct.

Cholangitis Infection within bile ducts.Usually secondary to obstruction of common bileduct.In 70% of patients, presents with Charcots triad.

RUQ pain Jaundice


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Fever

Pathophysiology. There are three types of stones.

o CholesterolMost common type.

o Pigment15% of stones.From calcium bilirubinate.Caused by diseases that increase red cell destruction.Also occur in:

Cirrhosis Parasitic infections.

o Mixed All are caused by crystallisation of bile.

o Contains fine balance of:LethicineBile acidsPhospholipids

o If the fine balance is disturbed by increases in any of the components, stasis and stonesare likely.

Sludge results from crystal formation, without large stones forming.o Unknown if it is the first step on the pathway to stones, or is an independent process.

Prevelence 1 2% of the population per year. At some point in a normal life will affect.

o 20% of womeno 14% of men.o 12.9% of men over 60o 22.4% of women over 60.

Risk factors.o Sex.

More common in women.Aeitiology may be secondary to

Variations in oestrogen causing increased cholesterol secretion Progesterone causing bile stasis.

Pregnant women more likely to have symptoms. Women with multiple pregnancies are at increased risk.

Oral contraceptive pill is also a risk factor/o Age.

Gall stones are rare in children. If they do, it is likely due to:

o Congenital abnormalitieso Biliary anomalieso Haemolytic pigment stones.

Incidence of gall stones increases by 1 3% per year.o Classically, risk factors are.

Fair FatFertileFemale


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o Elevated LFTsCBD stones suggested by raised.

ALT AST AP

Raised amylase suggests gall stone pancreatitis.

Imaging studies. US is best initial imaging.

o 95% sensitivity for stoneso 80% specific for cholecystitis

Thickened wallDistension

o 98% sensitive and specific for simple stones.o May show Pericholecystic fluido Can demonstrate sonographic Murphys sign.o Can demonstrate CBD dilatation to 7 8 mm.

CT and ERCP are useful adjuncts. X rays.

o 15% of stones are radio opaque.o Porcelain gall bladder may be seeno Air in biliary tree or wall may be seen.

Sign of emphesymatous gall bladder.Sign of infection.

o MRCP is gold standard imaging

ERCP is diagnostic and therapeutic.o Provides radioscopic and endoscopic visualization of biliary tree.o Indicated when CBD is dilated and LFTs are elevated.o Complications include.

BleedingPancreatitisPerforationCholangitis.

Acute care. Suspect biliary colic in patients with.

o RUQ of < 6 hour durationo Radiating to back

Consider acute cholecystitis in those with.o Longer duration of pain.o With or without fever.

Be vigilant in elderly patients and diabetics.o Dont tolerate delay in diagnosis.o Easily progress to sepsis.

Primary goal of acute care is diagnosis of acute cholecystitiso Hospitalisation is normally required.


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Resuscitate patient if necessary. Gain IV access

o Send blood tests.o Send blood cultures if febrile.o Replace volume with.

IV fluids Nasogastric feeding

Monitor.o Pulse oximetryo ECG

In patients who are unstable or in severe pain.o Consider bedside US to exclude AAA.o Assist in diagnosis of acute cholecystitis.

Administer pain control early.

Cholecystectomy can be performed.o After the first 24 48 hours.o After acute inflammation subsides.o Laproscopic cholecystectomy is very effective.

Complication rate of 4%5% convert to open proceduresAcutely, 50% end up being performed as open procedures.

More unstable patients require more urgent interventions.o Percutaneous drainageo ERCP

Complications of acute cholecystitis.Empyema of gall bladder Pus filled gall bladder due to bacterial proliferation in billiary

obstruction.Usually results in a more feverish, toxic picture.

Emphysematous cholecystitis More commonly in men and diabetics.Severe RUQ pain.Generalized sepsisImaging shows air in gall bladder wall or lumen

Perforated gall bladder Occurs in 10% of acute cholecystitis.Usually becomes contained abscess in RUQ.

Gallstone ileus UncommonPerforation of gall stone into adjacent viscus through cholecystoentericfistula.If stone is large enough, can cause small bowel obstruction.

Raynauds pentad. Charcots triad. RUQ pain Jaundice Fever

Altered mental stateSigns of shock.


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Choledocholithiasis.o Can present similarly to cholelithiasis.

With the addition of jaundice.o Differential diagnosis.

Cholelithiasis

HepatitisSclerosisng cholangitisCancer.

Less likely.o Treatment is with ERCP

Stone extractionSphincterotomy.

o Interval cholecystectomy after recovery from ERCP

Gallstone pancreatitis.o Cause of 35% of acute pancreatitis.o Pathophysiology.

Reflux of bile into pancreatic duct.Obstruction of ampulla by stone.

o Treatment.ResuscitateAnalgesiaIV fluidsOnce acute inflammation resolving.

ERCP to remove stone Sphincterotomy

Cholecystectomy before hospital discharge.

Acute Pancreatitis. Defined as reversible inflammation of the pancreas. Usually associated with.

o Severe, acute upper abdominal paino Elevated blood levels of pancreatic enzymes.

Can affect pancreatic tissues, or pancreatic tissues and distant organs. Mild disease is when disease only affects pancreatic tissue. Severe disease occurs when there are extra pancreatic complications.

Aetiology Incidence of 4.8 24.2 per 100,000 Mortality in hospitalized patients is about 10%.

o Ranges from 2 22%o In severe pancreatitis, mortality is 30%

Mortality in first 2 weeks normally due too SIRSo Organ failure


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Mortality after 2 weeks is normally due to sepsis. Causes.

o Idiopathic/ Infections 10%o Gall stones 30%o Ethanol 10%o Trauma/Tumor o Scorpion venomo Mumpso Auto immune

Eg. SLEo Steroidso High blood levels of.

TriglyceridesCalciumParathyroid hormone

o Drugs.Eg. thiazide diuretics.

Clinical presentation Acute onset, persistant upper abdominal pain.

o May radiate to back, chest and flanks. Nausea & vomiting Restlessness Bending forwards provides relief Signs.

o Fever o Hypotensiono Tachycardiao Severe abdominal tendernesso Peritoneal signso Abdominal distensiono Respiratory distresso Bruising


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Cullens sign Peri umbilical

Grey Turners sign Flanks

Foxs sign Inguinal ligament.

o If severe.Marked tendernessGuardingDistensionSigns of hypotension or shock JaundiceRespiratory findings.

Diagnosis Based on clinical picture and laboratory results. Important to do with first episode to determine aetiology.

o Lipase.

High sensitivity and specificity.o Amylaseo Calcium profileo Triglycerides.

Acute.Post resolution.

U&Es Creatinine CRP LFTs.

o ALT > 150 IU/Lo Specific for stones.

Urinalysis ABG

CT with contrast.o Standard technique.o Used with all with unclear diagnosiso Used at 72 hours in severe disease.

In accordance with APACHE II Acute Physiology and Chronic Health Evaluation.

Trans abdominal ultrasound.o Diagnostic in first episode.o

Helps determine aeitiology. MRCP

Prognosis.o Various scales for predicting prognosis have been used.o APACHE II score is often used.o CT severity index.

Most accurate predicting score for acute pancreatitis.o Ransons & Glasgow Scores are most commonly used.


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Glasgow. P: pO 2 < 8.4 kPa. A: Age > 55 years N: Neutrophils (WCC) > 15 x 10 9/L C: Calcium < 2 mmol/L

R: uRea > 16 mmol/L E: el dee aitch (LDH) > 600 units/L A: Albumin < 32 g/L

AST/ALT > 200 units S: Sugar > 10 mmol/L

Ransons On admission.

o Age > 55o WBC > 15 x 10 9/Lo Glucose > 10 mmol/Lo LDH > 600 units/Lo SGOT > 250 units/L

Within first 48 hours.o Haematocrit fall by < 10%o Urea increase > 8 mg/dlo Calcium < 8 mg/dlo PaO 2 < 60 mmHgo Base excess < 4 meg/Lo Estimated fluid sequestration > 600 ml.

Management. Monitor.

o Haemodynamicso Volume

Volume repletion Oxygen therapy Analgesia NG tube

o If vomiting Nutrition.

o Oral nutrition when toleratingo TPN for severe cases who dont settle.

If severe, consider.o Admit to ICUo Surgical debridement of any infected necrosis

Appendicits. Commonest abdominal emergency. Estimated to affect a sixth of the UK population at some point.

o Prevalent only in those who eat a Western diet.


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Pathology Usually occurs when appendix is

o Obstructed by faecolith or foreign body in the lumen.o Fibrous stricture within wall from previous inflammationo Enlargement of lymphoid follicles in wall.

Secondary to catarrhal inflammation of mucosao Outflow obstruction by CA caecum or ascending colon.

Occasionally.o Carcinoid tumour at base.

Rarely.

Obstructed appendix forms closed loop.o Bacteria proliferate in lumen and invade wall.o Wall damaged by pressure necrosiso End arteries supplying the appendix may become thrombosed

If this happens, gangrene and perforation is inevitable. No strict time period for development of gangrene.

o May perforate within 12 hours.o Rare to see acute appendicitis, without perforation, at 3 4 days.

Effects of appendicular obstruction depends on contents of the lumen.o Bacteria will cause acute inflammation.o Empty appendix will cause mucocele.

Goblet cells in wall continue to secrete mucous into lumen, but it cant escape. Appendicitis can occur in non obstructed appendix.

o Direct infection of lymphoid follicles.o Haematogenic infection.

Streptococcal appendicitisRare.

o Non obstructive appendicitis more likely to spontaneously resolve than obstructedform.

Appendicitis is rare at extremes of life.o Infant appendix is wide mouthed and well drained.o Elderly appendix is almost obliterated.

Is often diagnosed late and poorly tolerated when it does occur in these age groups.

Course.o Acutely inflammed appendix may spontaneously resolve.o Further attacks are likely.o Not uncommon for patient to report previous, milder attacks.

Grumbling appendixo More often, inflamed appendix becomes gangrenous and perforates causing either:

General peritonitis

Appendicular abscess.

Presentation. Classically, marked localised pain & tenderness in RIF. Pain


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o Hippocratic facies.Special investigations.

Leucocyte count increased.o Mild polymorph leucocytosis is the rule.

CT increasingly used to evaluate atypical presentations and complications. US of RIF.

o Diagnostic in experienced hands.

Generally investigations are for ruling out other differentials.

Differentials. Meckles diverticulitis is clinically indistinguishable from appendicitis.

o Investigate if appendix normal at surgery. Mesenteric adenitis.

o Particularly in childreno Often follows respiratory infection.o May co exist with appendicitis

Testicular torsion.o Vital to examine testicles in all males with abdominal pain.o Can also be maldescent.

RIF Masso Appendix abscess or masso Carcinoma of caecum.

Older age groupLonger historyOften causes diarrhoeaAnaemiaPositive Faecal Occult BloodsPositive barium enema

o

Crohns disease.First differential in young patients with mass and diarrhoea.o Gall bladder distension.

Common to extend down to RIF.o Pelvic kidney/ renal transplant.o Ovarian or tubal masso Aneurysm of common or external iliac arteryo Retroperitoneal tumour.

Soft tissues and lymph nodes of posterior abdominal wallPelvic organs.

o Ileocaecal tuberculosis.Rare in UK Common in India

o Psoas abscess. Now rare.


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Treatment. Appendectomy.

o

Normally performed laproscopically.o Only fully diagnostic procedure.

Immediate appendectomy is not indicated in the following situations.o Heavily moribund patient with advanced peritonitis.

Priority is IV fluids NG aspiration Antibiotics Resuscitation.

o Resolved appendicitis.Appendectomy should be performed as an elective procedure, rather than as an

immediate emergency.o Appendix mass present, but no evidence of peritonitis.o Where circumstances make operation difficult.

Eg. at sea.Reliance must be placed on conservative regimen.Better to hope for resolution or local abscess formation than to operate in lessthan ideal circumstances.

Antibiotic prophylaxis.o Given preoperatively.o If peritonitis found in theatre, antibiotics continued.o Cover aerobic and anaerobic bacteria.

Metronidazole + GentamicinCephalosporin

o Regimen may need to be changed in the light of culture & sensitivity of the pusTakes 24 48 hours.

Drain inserted post operatively.o If inflammation is severe.o If local abscess is presento If closure of appendix stump not perfectly sound.

Very rarely, inflammation and adherence is so severe that appendix cant be safely removed.o Insert good drainage.o Re attempt surgery in about 3 months.


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Appendix mass. Often patient will present with.

o RIF masso 4 5 days abdominal paino Otherwise soft, non tender abdomen.o Normal bowel sounds.o No evidence of generalized peritonitis.

This occurs when inflamed appendix is walled off by adhesions to momentum and adjacentviscera.

Immediate surgery in these circumstances is difficult. Treatment.

o Initial therapy is conservative.o Outlines of mass marked on skin.o Patient put on fluid dieto Vital signs carefully monitored.o Metronidazole is started.

Prolonged antibiotics are not indicated.Causes chronic inflammatory mass, honeycombed with abscess.

Antibioticoma.o 80% of patients will resolve on this therapy.

Send for elective appendectomy in 3 months.If appendectomy not performed

Significant risk of reoccurance.o Remaining cases will have enlarging masses and persistant pyrexia.

Institute drainage of abscess Neglected abscesses can perforate though to.

Exterior Rectum Abdominal cavity.

Appendicitis in pregnancy. Same incidence as in the general population. Higher morbidity and mortality.

o Often diagnosed late as confused with other complications of pregnancy. Has to be differentiated from.

o Pyelitiso Vomiting of pregnancyo Red degeneration of fibroido Torsion of ovarian cyst.

Appendix displaced superior lateral by enlarging uterus.o Pain and tenderness move appropriately.

Considerable danger of miscarriageo Particularly in first trimester.


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2. Is there an ileus or mechanical obstruction?o In functional obstruction due to reduced bowel motility (ileus)

No painAbsent bowel sounds.

o Paralytic ileus.Due to adynamic bowel due to absence of normal peristalsis.

Contributory factors. Abdominal surgery. Localised peritonitis Spinal injury Hypokalaemia Hyponatraemia Uraemia Peritoneal sepsis Drugs.

Eg. tricyclic antidepressants.o Pseudo obstruction.

Like mechanical obstruction, but with no cause for the obstruction.

When it occurs in the colon, known as Ogilvies syndromePredisposing factors.o Puerperiumo Pelvic surgeryo Traumao Cardiorespiratory disorders.Treatment.o Manage conservatively.o Neostigmine or colonoscopic decompressionare sometimes useful.In chronic pseudo obstruction, weight loss and malnutrition is a

problem.

3. Is the bowel strangulated?o Suspected if.

Patient more ill than you would expect.Pain is sharper and more constant.Pain tends to be localised.Cardinal sign is peritonismMay be:

Fever High WCC


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Mesenteric ischaemia

Management.o General principles.

Definitive treatment determined by.

Site Speed of onset Completeness of obstruction.

Strangulation and large bowel obstruction require rapid surgery.Ileus and incomplete small bowel obstruction can be initially managedconservatively.

o Immediate action.Drip and Suck

NG tube aspirationo Simply putting patient NBM doesnt properly rest bowel.o Intestine can produce 9L of fluid per day on its own.

IV fluid

Rehydrate Correct electrolyte imbalance.

o Further imaging.Case for colonoscopy in some causes of mechanical obstruction.

Risk of perforationFollow through with water soluble contrast (eg. Gastrografin) may be helpful indetermining level of obstruction.

Also some therapeutic action against mild mechanical obstruction.CT may show.Fluid filled bowelTransition zone at site of obstruction.

o

Surgery. Strangulation requires emergency surgery. As does closed loop obstruction

Closed loop obstruction. Large bowel obstruction. Ileocaecal valve remains patent, preventing reflux back. Large pressure builds up between valve and obstruction.

Tenderness over grossly distended bowel.


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Sections > 12 cm require urgent decompression.For less severe obstruction.

Water sodium enema Clears obstruction and restores fluid balance.

Small bowel obstruction secondary to adhesions rarely requires surgery.

Hernias.

Differential diagnosis of groin pain/ swelling. Consider differentials in terms of anatomical layers.

o Hernial orifices.Inguinal herniasFemoral hernias

o Testicular apparatusHydrocele of the cordEctopic testes

o VeinSephena varix

o

Artery Femoral aneurysmo Lymphadenopathy, due to:

Infection NeoplasmLymphoma

o Psoas sheathPsoas abscess

o Skin and subcutaneous tissueLipoma

Definition of hernia Protrusion of an organ, or part of an organ, through a defect in the wall of the cavity that usually

contains it, into an abnormal position. Usually used with reference to abdominal contents.

Stages of hernia. Hernias can progress from being reducible to irreducible to being strangulated. Reducible.

o Contents can be returned entirely to the peritoneal cavity.o Clinical features:


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Lump. May disappear on lying down Usually not painful

o May cause some discomfort Cough impulse

Irreducible.o Contents can no longer be returned to the abdominal cavity.o Normally due to adhesions between the loops of bowel, causing a mass to form that is

larger than the neck of the hernia.o Sometimes inspissated faeces within the loops of bowel prevent reduction.o Clinical features:

Lump that will not disappear. Normally painless

No other symptoms.Absence of cough impulse doesnt necessarily mean strangulation.

Eg. irreducible femoral hernias often have no cough impulse due to theneck being blocked with omentum.

Strangulated.o Contents of hernia constricted by the neck of the sac to a degree where circulation is cut

off.Gangrene is inevitable if constriction not relieved.If gut is involved, gangrene and necrosis will cause perforation and peritonitis.

o Clinical features.Sudden onset of:

Severe pain in hernia. Central, colicky pain

Signs of internal obstruction. Vomiting Abdominal distension Absolute constipation

Examination Lump

o Tender o Tenseo Non reducibleo No cough impulse

Overlying skin becomes.o Inflammedo Oedematous

Abdominal tenderness Noisy bowel sounds. Intestinal obstruction.

Features are less marked when it is momentum that has herniated, rather than bowel.

o The hernias that commonly strangulate, in order of decreasing frequency are:Femoral


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Indirect inguinalUmbillical

Risk Factors Weakening of the muscles or membranes.

o Increasing age.

Eg. degeneration of annulus fibrosis of intervertebral disc.o Genetic conditions.

Ehlers Danlos syndromeMarfan syndrome

o Stretching of muscles during pregnancyo Rapid weight loss.o Scars from previous surgery.

Chronic increase in intra abdominal pressure.o Pregnancyo Asciteso COPDo Dyschezia

Suppressing defecationo Benign prostatic hypertension

Anatomical defects and why they exist Can be congenital or acquired Congenital.

o Normal, or formerly normal, defect.Congenital indirect inguinal hernia forming through patent processus vaginalis.

Inguinal hernias. Classified into indirect or direct.

Indirect DirectOrigin Enters internal inguinal ring.

Transverses inguinal canalExits external inguinal ring.

Perforates through posterior wallof inguinal canal, medial toinferior epigastric vessels.

Congenital or acquired May be congenital Always acquired.Rare in childhood andadolescence.

Controlled by pressure over internal ring

Yes No

Strangulates Commonly, because of narrowneck at internal ring

Rarely, because of wide neck

Extends into scrotum Often RarelyReduces on lying Not readily SpontaneouslyRecurs after surgery Uncommon More common

Knowledge of the anatomy of the inguinal canal is important in understanding these hernias.o Represents oblique passage taken through the lower abdominal wall by:

Testis and cord/ round uterine ligamentIlioinguinal nerve

o About 4 cm long.o Passes inferomedially and deep to superficial.o Demarkated at each end by internal and external inguinal rings.o Lies parallel to, and immediately superficial to, inguinal ligament.o Its borders are:


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Direct inguinal hernia.o Pushes its way through posterior wall of inguinal canal.o Because it lies medially to internal inguinal ring, is not controlled by pressure at this

point.o Can be distinguished from indirect hernia by:

On inspection, direct hernia protrudes directly forward rather than obliquely.Direct hernias are always acquired.

Very rare in infancy or adolescenceDirect hernias have very large necks, compared to indirect.

Strangulation is rare.o Although clinically it is normally easy to distinguish between indirect and direct hernias,

ultimate differention is only possible on operation.Epigastric vessels demarcate medial edge of internal inguinal ring.

Direct hernias pass medially to thiso Through Hesselbachs triangle.

Superiolaterally: Epigastric vessels

Inferiorly: Inguinal ligamanet

Medially: Rectus abdominus

Indirect hernias pass laterally to this.o It is common for indirect and direct hernias to co exist.

Bulging around both sides of epigastric vessles. Distribution of inguinal hernias.

o 60% occur on the right.o 20% occur on the lefto 20% occur bilaterally.

Treatment.o Congenital inguinal hernias always need operation.

Herniotomy performed at about 1 year old. Patent processus vaginalis is ligated. Hernial sac excised.

o Adults normally advised to have surgery.Excision of sac.Repair of weakened inguinal canal..

o Surgical technique.Shouldice repair.

Plication of the transversalis fascia in posterior wall, using a nylonsuture.

Lichtenstein repair. Reinforcement of posterior wall with nylon or polypropylene mesh.

Laproscopically. Cover hernial orifice with mesh from the inside. Particularly useful in recurrent or bilateral hernias.

o Truss is only useful in patients who are too generally unwell for surgery.


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Often difficult to keep truss in place.o Even in unwell patients, if a patient has a painful hernia that may strangulate it is better to

risk surgery electively than to run the risk of being forced to go to surgery as anemergency.

o Recurrent inguinal hernia may be due to:Infection

HaematomaPoor surgical repair technique.Continuing increased abdominal pressure.

Constipation CA bowel Bladder neck obstruction Large prostate.

Umbillical hernia Two forms.

o Congential umbilical herniao Exomphalos

Congenital umbilical hernia.o Result of failure of complete closure of umbilical cicatrix.o Especially common in black children.o Vast majority resolve spontaneously in first year of life.o Treatment.

Surgery should not be performed when under 2, due to high likelihood of spontaneous resolution.Main management is reassurance of parents and safety netting if it hasntdisappeared by the age of two.Strapping the hernia or providing a truss allay parental concerns, but no realimpact on hernia resolution.

Exomphalos.o Rare condition.o Failure of all, or part, of the midgut to return to the abdominal cavity in utero.o At birth, bowel is contained in translucent sac, protruding through defective abdominal

wall.o Untreated, the sac ruptures causing fatal peritonitis.

Rupture during delivery is common, so check for it on in utero US scans.o Management.

Immediate surgical repair if possible.If sac is massive.

Cover in dressing soaked in mild antiseptic. Gradual epithelialisation will occur, allowing repair at a later date.

Acquired Hernias. Weakness in the abdominal wall due to

o Passage of structures exiting the abdominal cavity.


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Closure of femoral canal.o Invasive management needed due to risk and danger of

strangulation.o Closure of the canal is usually by suturing a ball of

polypropylene mesh into the hole.

Complications Post surgery, complications include rejection of the mesh.

o Obvious, sometimes localised, swelling and pain.o Normally requires mesh removal

Continuous discharge from scar is normal for a while after mesh removal Untreated hernia may become complicated by:

o Inflammationo Irreducibilityo Obstructiono Strangulationo Hydocele

Remnant of peritoneum from tunica vaginalis secretes serous fluid into thecavity.o Haemorrhage

Aneurysms. Defined as an artery dilating to > 150% of normal. Ongoing process True aneurysms are actual dilatations of blood vessels. False aneurysms are collections of blood around vessel wall that communicates with the lumen.

o Eg. following trauma. Aneurysms may be:

o Fusiformo Saccular


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Are expansile on palpation, rather than just pulsatile.

Pathophysiology.o Atheromatous degeneration is main contributing factor.o Other factors include.

Connective tissue disorders. Marfans Ehlers Danlos

Infections. Mycotic aneurysms Tertiary syphilis

Factors leading to Cystic medial necrosis Mainly in AAA. Immune responses Biochemical wall stress Shifts in balance of remodelling.

o Causes proteolytic degeneration of aortic wall.o Eg. Increased metalloprotease activity.

Inflammation.o Increased lymphocyte and macrophage infiltration.

Molecular genetics.o Eg. extracellular matrix protein degradation.

Common sites.o Aortao Illiac arterieso Femoral arterieso Popilteal arteries

Complications.o Rupture

Mortality from ruptured AAA increases with age.125/million in those 55 59 years2728/million in those > 85 years.

o Thrombosiso Embolismo Pressure on other structures.

Clinical pictures.o Intermittent or continuous abdominal pain.o Radiation to back.

Also can radiate to iliac fossae or groins.Dont dismiss as renal colic.

o Collapse


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o Complications.Spinal ischemiaMesenteric ischemiaDistal trash from dislodged thrombus debris.

o Studies show that age > 80 is not a reason to decline surgery. Stenting.

o Major operations can sometimes be avoided by inserting an endovascular stent viafemoral artery.

o Compared with conventional surgery.Shorter hospital stays.Fewer transfusions.

o Require lifelong monitoring.o Suitability not increased by early detection and monitoring.o Suitability apparently determined much earlier in aneurysm life than when it would be

picked up on by AAA surveillance programs.

Thoracic aortic dissection. Blood splits aortic media with sudden, tearing chest pain.

o May radiate to back. As dissection unfolds, leads to occlusion of branches sequentially.

o Carotid artery.HemiplegiaUnequal arm pulses and BP

o Anterior spinal artery.Paraplegia

o Renal artery.Anuria.

o If dissection spreads proximally.Aortic incompetenceInferior MI

Type A dissections affect solely the ascending aorta. Type B dissections affect the descending aorta. All patients with Type A dissection require.

o Consider surgeryo Get emergency cardiothoracic advice.

Management.o Cross match 10 units of blood.o ECGo CXR

Expanded mediastinum is rare.o CT/MRI or transoesophageal echocardiogram (TOE).o Take to ITU.o Give hypotensives to keep SBP = 100 110 mmHg.o IV infusion of Labetalol or esmolol can be helpful.o Acute operative mortality is < 25%.

Documents

Abdominal Pain for Medical Finals (based on Newcastle university learning outcomes)