Yr 2 Abdominal Pain

8/8/2019 Yr 2 Abdominal Pain

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The perception of pain is subjective and differs

greatly between patients. As a simple rule of

thumb, pain is what the patient says it is.

to ask the patient to rate his pain on an

imaginary scale of 010, with 0 meaning no

pain at all and 10 the worst pain ever.


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Physiology of acute pain

Nocioceptors are the sensory receptors for pain and arenerve endings, whichexist in almost all tissues. These nerveendings are damaged or stimulated by chemical mediatorsand transmit signals via afferent sensory pathways to the

central nervous system (dorsal horn, contralateral spino-thalamic tracts, thalamus and cortex).

Small myelinated A-delta fibres conduct fast pain (localised,sharp pain).

larger unmyelinated C fibres conduct slow pain (diffuse,

dull pain) from the peripheries. Visceral pain is poorlylocalised and associated with autonomic symptoms.


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The gate control theory of pain describes

how synaptic transmission can be modified at

the dorsal horn by stimulating other afferent

sensory pathways.

rubbing or applying transcutaneous nerve

stimulation (TENS).


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The physiological

effects of severe pain include:

Tachycardia, hypertension and increased

myocardial oxygen demand Nausea and vomiting, ileus

Reduced vital capacity, difficulty coughing, basalatelectasis and chest

infections Urinary retention

Thromboembolism.


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Abdominal pain

a subjective unpleasant sensation felt in any

of the abdominal regions. which may beAcute

(sudden onset) or chronic (persists for longer

than a few days and may he present intermit-

tently for months or years).

Referredpain is the perception of pain in an

area remote from the site of origin of the pain


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The level of abdominal pain generally relates to the origin:

foregut = upper: midgut = middle; hindgut =lower.

Generally

colicky (visceral) pain - stretching or contracting ahollow viscus (e.g. gallbladder. ureter, ileum).

constant localized (somatic) pain - peritoneal irritationand indicates the presence of inflammation/ infection(e.g. pancreatitis, cholecystitis. appendicitis).

very severe pain - ischaemia or general-ized peritonitis

(e.g. mesenteric infarction. perforated duodenal ulcer). Referredcauses ofpain: pneumonia (right lower lobe),

myocardial infarction. lumbar nerve root pathology.


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History When did the pain start? gradually or suddenly? sort of pain is

it? Aching, sharp, burning, etc?

constant or variable? `colicky' (waxes and wanes in cycles)?

exacerbates/precipitates the pain (movement, posture,

eating)? alleviates the pain?

associated symptoms (vomiting, diarrhoea, acid reflux, back

pain, breathlessness, GI bleeding, dysuria, haematuria)?

previous episodes? When and how frequently?

Any recent change in bowel habit?

any symptoms of indigestion, steatorrhoea or weight loss?


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Past medical history

any significant medical conditions.any history of previous abdominal

surgery.

Drugs that might cause pain (e.g.

NSAIDs and peptic ulceration) or

mask abdominal signs (e.g.corticosteroids).

Consider alcohol as a cause of the

pain (e.g. pancreatitis).

Examination

Is the patient well or unwell?

Comfortable or uncomfortable?

Still or restless?

Eyes open (fearfully watching the

doctor's abdominal examination?) or

closed and relaxed?

Is there fever, anaemia, jaundice,lymphadenopathy, evi-dence of

weight loss, malnutrition, foetor,

ketosis?

Are they dehydrated, shocked,

hypovolaemic?

Do they have an acute abdomen?

Could there be obstruction

(distension, vomiting, absolute

constipation, high-pitched tinkling

bowel sounds)?

Is there tenderness, guarding, rigidity,rebound, visible peristalsis?

Might there be enlargement of aorta,

liver, kidney, spleen, gallbladder,

hernias, other masses


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ACUTE ABDOMEN

A sudden, severe abdominal pain that is less

than 24 hours in duration. It is in many cases

an emergent condition requiring urgent and

specific diagnosis which may or may not

require immediate surgical treatment.


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10 Features of pain

site (ask the patient to point with one finger; has the

site of pain changed?) severity (compared to previous experiences)

characteristics (e.g. sharp, burning, gnawing, dull)

radiation (e.g. to back, around abdominal wall into

groin) onset (e.g. sudden, gradual, time of day)

periodicity (over minutes, hours)


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relieving factors (e.g. movement, vomiting,

lying still, leaning forwards) exacerbating factors (e.g. movement, drinking

fluids)

associated features (e.g. nausea, vomiting,

changes in colour of urine, stool or skin)

previous episodes (hours/days/weeks/yearsago; more/less severe; diagnosis then?)


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Pathways of visceral

innervation.

The afferent fibers

mediating pain travelwith the autonomic

neurons to

communicate with the

central nervous

system where pain isperceived. The vagal

and pelvic nerves are

parasympathetic

fibers, whereas those

from the thoracic andlumbar groups are

sympathetic.


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Neuroanatomicpathway mediating

visceral pain.

The pathway from

sensation in an

abdominal viscus to

perception of pain in

the thalamus,

somatosensory cortex,

limbic system and

frontal lobes.


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Mode of onset

ofPAIN

A sudden onset an intra-abdominal

catastrophe,

a ruptured abdominal aortic aneurysm,

a perforated viscus, or

a ruptured ectopic pregnancy.

Rapidly progressive pain that becomes intensely

centered in a well-defined area within a period of afew minutes to an hour or two

acute cholecystitis, pancreatitis, or mesenteric

thrombosis.


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A gradual onset over several hours, usually

beginning as slight or vague discomfort and slowly

progressing to steady and more localized pain -

subacute process ( characteristic of peritoneal

inflammation. )

acute appendicitis,

diverticulitis,

pelvic inflammatory disease (PID),

incarcerated hernias, and intestinal obstruction.


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Pain either intermittent or continuous.

Intermittent or cramping pain (colic)

pain that occurs for a short period (a few

minutes), followed by longer periods (a few

minutes to one-half hour) of complete remission

during which there is no pain at all.

obstruction of a hollow viscus and results from

vigorous peristalsis in the wall of the viscus

proximal to the site of obstruction.


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perceived as deep in the abdomen and ispoorly localized. The patient is restless, maywrithe about incessantly in an effort to finda comfortable position, and often presses on

the abdominal wall in an attempt toalleviate the pain.

the intermittent pain associated with intestinalobstruction typically described as gripping and

mounting is usually severe but bearable


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the pain associated with obstruction of small

conduits (e.g., the biliary tract, the ureters,

and the uterine tubes) often becomes

unbearable.

Obstruction of the gallbladder or bile ducts

gives rise to a type of pain often referred to

as biliary colic; (a misnomer, in that biliary

pain is usually constant because of the lack of

a strong muscular coat in the biliary tree andthe absence of regular peristalsis.)


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Continuous orconstant pain

present for hours or days without any

period of complete relief usually indicative

of peritoneal Inflammation or ischemia. It

may be of steady intensity throughout, or it

may be associated with intermittent pain.


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The typical colicky pain associated with simpleintestinal obstruction changes when strangulation

occurs, becoming continuous pain that persistsbetween episodes or waves of cramping pain.

Typical of certain pathological states

the general burning pain of a perforated gastric ulcer,

the tearing pain of a dissecting aneurysm, and

the gripping pain of intestinal obstruction.


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The character of the pain is not always a reliable clueto its cause. For several reasonsatypical painpatterns, dual innervation by visceral and somaticafferents, normal variations in organ position, and

widely diverse underlying pathological statesthelocationofabdominal pain is only a rough guide todiagnosis.

nevertheless the pain tends to occur in characteristiclocations, such as the right upper quadrant(cholecystitis), the right lower quadrant(appendicitis), the epigastrium (pancreatitis), or theleft lower quadrant (sigmoid diverticulitis)


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Important to determine the location ofthe pain at

onset because this maydifferfrom the location at the

time ofpresentation (so-calledshifting pain).

In fact, the chronological sequence of events in the

patients history is often more important for

diagnosis than the location of the pain alone.

the classic pain of appendicitis begins in the

periumbilical region and settles in the right

lower quadrant.


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Locations for pain related to conditions causing an acute

abdomen.

Biliary colic may radiate to the back or shoulder (dotted

line).


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Patterns of referral of pain of abdominal origin: anterior

Pain of abdominal origin tends to be referred in characteristic patterns. The more

severe the pain is, the more likely it is to be referred. Shown are the anterior areas

of referred pain

Oesophagus

Stomach

Liver and

Gallbladder

Pylorus

Colon

Left and Right

Kidneys

Ureter


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Oesophageal pain

many patterns:

Burning ) Gripping )

Pressing )

Boring )

Stabbing )

Usually in the anterior

chest, it tends to be felt

mainly in the throat orepigastrium and sometimes

radiates to the neck, back,

or upper armsall of

which may equally apply tocardiac pain.


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odynophagia,

discomfort or pain on swallowing hot or coldliquids and, occasionally, alcohol.


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Gall Bladder/Stone

is usually felt as a severe gripping or gnawing painin the right upper quadrant.

may radiate to the epigastrium, or around thelower ribs, or directly through to the back.

maybe referred to the lower pole of the scapulaor the right lower ribs posteriorly, lasting for 20minutes to 6 hours

variations ~ retrosternal pain and abdominalpainonly in the epigastrium or on the left side.

Acute cholecystitis x Severe pain and tendernessin right subcostal region for > 12 hours

Obstructive jaundice with or without pain


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Acalculous biliary pain

Occasionally, biliary colic seems to be

associated with a high pressure sphincter of

Oddi, and symptoms may resolve after

endoscopic sphincterotomy.


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Cancer of the stomach

Epigastric pain is present in about 80% of

patients and may be similar to that from a

benign gastric ulcer. If caused by obstruction

of the gastric lumen, it is relieved by vomiting.

Constant abdominal pain, and particularly

back pain, are sinister symptoms implying

local invasion by tumour


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pancreatic cancer

epigastric discomfort or dull back pain.


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functional dyspepsia

Anorexia, nausea, and vomiting with pain can

all be regarded teleologically as protective

reflexes whereby the body prevents the entry

of toxins into the body.

also reduce the passage of chyme through

diseased parts of the upper gut, thereby

minimising further pain.


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Nausea, vomiting and pain

Toxins and hypertonic saline induce vomiting by

stimulating afferent serotonergic nerves in the

vagus that connect with the chemoreceptive

trigger zone in the floor of the fourth ventricle ofthe brain.

These afferent nerves can also respond to acid,

amino acids, and fatty acids. 5-HT3 receptor antagonists act on the vagal

afferents to reduce nausea and emesis.


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Excessive distension of the gut will induce pain

via serosal stretch receptors whose output

passes via sympathetic neurones to the

central nervous system

while ulcers cause acid related pain mostly via

vagal afferents.


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causes of anorexia, nausea, vomiting, and pain

Commonest - duodenalulcer disease, functionaldyspepsia and irritablebowel syndrome.

Gastric ulcer, gastro-oesophageal reflux, gastriccancer, and gall stones 5-10% each

rarer diseases - diverticulardisease, small intestinal

Crohns disease, coloncancer, pancreatitis

Pregnancy a mysteriouscause of nausea andvomiting.

Hepatitis during its prodrome

misleading, but the

appearance of jaundice makes

all clear.

Even rarer - metabolic diseases

~ diabetic ketoacidosis, renaltubular acidosis, and

adrenocortical insufficiency ,

hypercalcaemia, acidosis or

alkalosis

drug induced nausea -NSAIDs,

opiates, antibiotics, hormone

preparations, and

chemotherapeutic agents.


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Possible reasons for anorexia, nausea, and

vomiting with pain


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Investigations

FBC: leucocytosis. infective/inflammatorydiseases, anaemia, occult malignancy, pepticulcer disease.

LFTs: usually abnormal in cholangitis, may heabnormal in acute cholecystitis.

Amylase: serum level > 1000iu diagnostic ofpancreatitis. Serum level 500 - 1000 iu.?pancreatitis, perforated ulcer, bowel ischaemia,

severe sepsis. Serum level raised


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Arterial blood gases: metabolic acidosis?bowelischaemia, peritonitis, pancreatitis.

MSU: urinary tract infection (+/-ve nitrites, blood,protein). renal stone (++ve blood).

ECG: myocardial infarction. Chest X-ray: perforated viscus (free gas), pneumonia.

Abdominal X-ray: ischaemic bowel (dilated, thickenedoedematous loops). pancreatitis ('sentinel' dilated

upper jejunum). cholangitis (air in biliary tree), acutecolitis (dilated. oedematous. featureless colon). acuteobstruction, renal stones (radiodense opacity in renaltract).


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Ultrasound: intra-abdominal abscesses(diverticular. appendicular, pelvic), acutecholecystitis/empyema. ovarian pathology (cyst,

ectopic pregnancy), trauma (liver/spleenhaematoma). renal infections.

OGD: ?peptic ulcer.

CT scan: pancreatitis, trauma

(liver/spleen/mesenteric injuries). diverticulitis?.leaking aortic aneurysm.

IVU: renal stones, renal tract obstruction.


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JAUNDICE

Associate Professor Dr Sein Win

M.B.,B.S.(Ygn), M.Med.Sc.(Surgery)

Department of SurgeryFaculty of Medicine & Health Sciences, UNIMAS


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JAUNDICE


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Enterohepatic circulation of bile salts. Each

molecule circulates at least once for each meal


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Jaundice (icterus)

yellowing of the skin and sclera from accumu-lation of the pigment bilirubin in the bloodand tissues.

The bilirubin level has to exceed 35-40 mmol/l(2mg%) before jaundice is clinically apparent.

Kernicterus bilirubin staining of the Basalganglia, brain stem and cerebellum (musclespasticity/hypotonia, impaired vertical gaze,deafness. (impair Blood-brain barrier inneonates)


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Hyperbilirubinaemia is defined as a bilirubin

concentration above the normal laboratory

upper limit of 19 mol/l. Jaundice occurs when

bilirubin becomes visible within the sclera,

skin, and mucous membranes, at a blood

concentration of around 40 mol/l.


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INTRALUMINAL

Infestation

Clonorc his

Schistosomiasis

Gallstones

CAUSES OF OBSTRUCTIVE

JAUNDICE

EXTRINSIC

Portal lymphadenopathyChronic pancreatltis

Pancreatic tumour

Ampullary tumour

Duodenaltumour

MURAL/INTRINSICLiver cell transport

abnormalities

Sclerosing Cholangitis

Cholangiocarcinoma

Mirrizi syndrome

Benign stricturePostinflammatory

Postoperative

Postradiotherapy


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Classification

pre-hepatic

hepatic

post-hepatic (most of the surgically treatablecauses of jaundice)


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Pre-hepatic jaundice

Haemolytic/congenital hyperbilirubinaemias

Excess production of unconjugated bilirubin

exhausts the capacity of the liver to conjugate

the extra load.

Haemolytic anaemias (e.g. hereditary

spherocytosis. sickle cell disease,

Hypersplenism

Thalassaemia


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Hepatic/hepatocellular jaundice

Hepatic unconjugatedhyperbilirubinaemia

Failure of transport of unconjugated bilirubin into thecell, e.g. Gilbert's syndrome.

Failure of glucuronyl transferase activity. e.g.

Criglar-Najjar syndrome

Hepatic conjugatedhyperbilirubinaemia

Hepatocellular injury. Hepatocyte injury results in

failure of excretion of bilirubin. e.g. infections: viralhepatitis: poisons: aflatoxin: drugs: paracetamol,halothane.


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Post-hepatic/obstructive jaundice

post-hepatic conjugatedhyperbilirubinaemia

Anything that blocks the release of conjugated

bilirubin

From the hepatocyte or prevents its delivery

to the duodenum.


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Courvoisier's law.

'A palpable gallbladder in the presence of

jaundice is unlikely to be due to gallstones.

It usually indicates the presence of a

neoplastic stricture (tumour of pancreas,

ampulla. duodenum. CBD). chronic

pancreatitic stricture or portal

lymphadenopathy.


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Investigations FBC: haemolysis.

LFTs: I.

alkaline phosphatase (cholestasis), K-GT andtransaminases(hepatocellular).

Clotting: PT (elevated in cholestatic and bepatocellularjaundice).

Viral titres: hepatitis A, B. C. CMV. EBV.

Ultrasound: dilatation of the biliary tree (cholestasis),gall-stones (gallbladder and bile ducts), details ofhepatic parenchyma.

ERCP: bile duct strictures (tumours, pancreatitis,

inflam-matory), gallstones. Allows diagnosticbiopsy/cytology. Allows therapeutic stenting, stoneremoval.

PTC: similar to ERCP (useful where ERCP has failed).

Liver biopsy: hepatocellular disease.


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History

When was the jaundice first noticed and bywhom?

What does the patient mean by jaundice?

Are there any other symptoms (abdominal pain,

fever, weight loss, anorexia, steatorrhoea, darkurine, pruritus)?

Any travel? Consider malaria or infectioushepatitis.

Any features suggesting malignancy (e.g. weightloss, back pain), chronic liver disease (e.g.abdominal swelling due to ascites) or infectivehepatitis?


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History that should be taken from patients

presenting with jaundice

Duration of jaundice

Previous attacks ofjaundice

Pain

Chills, fever, systemicsymptoms

Itching

Exposure to drugs(prescribed and illegal)

Biliary surgery

Anorexia, weight loss

Colour of urine andstool

Contact with otherjaundiced patients

History of injections orblood transfusions

Occupation


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Past medical history

previous jaundice

known viral hepatitis

chronic liver disease or malignancy Is there

any history of blood transfusions

any anaesthetics (especially halothane)

known gallstones or previous cholecystectomy


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Drugs

all medication, prescribed, illicit and alternative,

as potential cause of jaundice.

Alcohol

patient's consumption of alcohol? Is the patient

dependent on alcohol?

Family history inherited causes of jaundice (e.g. haemolytic

anaemias, Gilbert's syndrome).


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Examination

Is the patient jaundiced? Look at sclerae.

signs of anaemia?

signs of weight loss, chronic liver disease? Any excoriations (suggesting pruritus)?

Is there hepatomegaly, splenomegaly or both?

a palpable gallbladder? any abdominal masses or tenderness?

Any there features of portal hypertension?


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Examination of patients with jaundice

Depth of jaundice

Scratch marks

Signs of chronic liver

disease: Palmar erythema

Clubbing

White nails

Dupuytren's contracture

Gynaecomastia

Liver:

Size

Shape

Surface

Enlargement of gall

bladder

Splenomegaly

Abdominal mass

Colour of urine and stool


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Liver function tests

markers of function - (albumin and bilirubin) markers of liver damage (alanine transaminase,

alkaline phosphatase, and Kglutamyl transferase).

a predominant rise in alanine transaminase activity(normally contained within the hepatocytes) suggests ahepatic process.

Serum transaminase activity is not usually raised inpatients with obstructive jaundice,

with common duct stones and cholangitis a mixedpicture of raised biliary and hepatic enzyme activity isoften seen.


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Epithelial cells lining the bile canaliculi

produce alkaline phosphatase, and its serum

activity is raised in patients with intrahepatic

cholestasis, cholangitis, or extrahepaticobstruction;

increased activity may also occur in patients

with focal hepatic lesions in the absence ofjaundice.


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In cholangitis with incomplete extrahepatic

obstruction, patients may have normal or

slightly raised serum bilirubin concentrations

and high serum alkaline phosphatase activity

Serum alkaline phosphatase is also produced

in bone, and bone disease may complicate the

interpretation of abnormal alkaline phos-phatase activity.


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The presence of a low serum albumin

concentration in a jaundiced patient suggests

a chronic disease process

Ch i i d f i h j di


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Changes in urine and faeces with jaundice

Cause of jaundice

Substance and site HaemolysisObstruction orcholestasis

Hepatocellular liverdisease

Urine

Bilirubin (conjugated) Normal* Raised Normal or raised

Urobilinogen Raised Absent or decreased Normal or raised

Faeces

Stercobilinogen Raised Absent or decreased Normal

Causes Haemolytic anaemia Extrahepatic biliary

obstruction (e.g.

gallstones, carcinoma

of pancreas or bile

duct, strictures of the

bile duct), intrahepatic

cholestasis (e.g. drugs,

recurrent) jaundice of

pregnancy)

Hepatitis, cirrhosis,

drugs, venous

obstruction


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Laboratory investigation


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Management of the Trauma Patient

. Primary Survey of the Trauma

PatientOngoing assessment and treatment

Secondary survey APenetrating Abdominal

Trauma

Gun shot wounds Stab wounds and other

penetrating abdominal trauma BluntAbdominal Trauma


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Head Trauma

Thoracic Trauma

Tension Pneumothorax

Flail Chest

MassiveHemothorax

Cardiac contusions Pulmonary contusions

Cardiac Tamponade

Blunt Abdominal Trauma

Penetrating Abdominal Trauma

Peripheral Arterial OcclusiveDisease

Peripheral Arterial OcclusiveDisease

Abdominal Aortic Aneurysms

Pelvic fracture Traumaticesophageal injuries Burns

Epistaxis

Acute Abdomen

Upper Gastrointestinal Bleeding

Lower Gastrointestinal Bleeding

Anorectal Disorders

Orthopedic Fractures andDislocations UrologicDisorders

Yr 2 Abdominal Pain

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