A PATIENT WITH A BIG

SPLEEN
Students: BYARUHANGA ISAAC 19/U/0804
MWAGALE SADAT 21/U/23473/PS
OKOT ANTHONY 19/U/28367

Tutor: Dr. Rejani Lalitha Opio

 Objectives

1. To know about the history and examination findings of a patient with a big
spleen.
2. To describe the microscopic and macroscopic structure of the spleen.
3. To describe the functions of the spleen.
4. To list the classification of splenomegaly.
5. To describe the aetiology of splenomegaly.
6. To explain the pathophysiology of splenomegaly.
7. To list the management of splenomegaly.
8. To explain the complications of splenomegaly.
Patient presentation
Who is the Patient?
Name: Mr Tulyamulebu Talent
Age; 17 years
Sex: Male
Address: Salama
Occupation: No work
N.O.K: Nanakula Jenifer ( mother)
D.O.A: 25TH March 2022
R.R: Self referral
What is the disease that the patient
has?
Presenting complaints
 Vomiting blood x 3/7
 Abdominal pain x 3/7
History of Presenting Complaints
Tulgamuleba Talent a 17 year old male, sero negative from Salama road; with portal
hypertension and episodes of bleeding varices in past three 3 years presented with a 3- day
history of vomiting blood of sudden onset. The vomitus contained fresh blood with some
clots but non smelly associated with dizziness, palpitations, no chest pain, no lower limb
swelling. Also presented with 3 day history of a gradual dull abdominal radiating to the left
shoulder and umbilical region, with no aggravating or relieving factors. He also presented
with a long standing history of yellow eyes for 3 years associated with passing dark yellow
urine. No itching of skin but with dark lose stool for 3 days. He also reported low grade
fever and chills that set in 2 days before vomiting started and associated poor appetite and
weight lose.
Review of systemsss

CVS: hx. palpitations, easy fatiguability, no chest pain, no paroxysmal nocturnal

dyspnoea, no orthopnoea, no lower limb swilling.
RS: DIB on walking, no cough, no noisy breath sounds, no haemoptysis.
C.N.S: severe dizziness, intermittent headaches, low grade fevers and chills, no
loss of consciousness, no convulsions, no loss of memory, no vision and no hearing
problems.
Musculo-skeletal: joint and muscle weakness, no joint pain, no muscle pain, no
swelling.
Genital-urinary: no polyuria, no dysuria, no urgency and frequency, no urinary
retention, no urethra discharge
E.N.T: no ear secretions, no nose secretions
Past Medical History: He was first diagnosed with the first episodes of bleeding varices in
2019 at Kirudu Hospital. He also had a second episode in 2021 both were managed by
blood transfusion, Trenexamic acid, propranolol and lactose. This is the third episode
which was first managed from emergency section by transfusion of 2 units of whole
blood, injections of trenexamic acid and then transferred to ward. No hx of any chronic
illness, no drug and food allergies.
Family History: He is a 2nd born in a family of 6 children all are alive, both parents are
alive. There is no history of family chronic illness.
Social-economical history: He has not been in school for 3 years now, assists his father
to do building when his stable. He is financially supported by both parents. He doesn’t
smoke or take alcohol. His fear is that the condition is recurrent and he expect to be
operated this time.
Summary: Tulyamuleba Talent a 17 year old male, sero negative with portal
hypertension presented with 3 day history of vomiting blood of sudden onset associated
with dizziness, palpitations, no chest pain, no lower limb swelling also presented with a
gradual dull abdominal pain radiating to the left shoulder and umbilical region, with
slight abdominal distention and no constipation.
Differential diagnosis:
 Portal hypertension with bleeding varices in view of vomiting of blood and atrium history of
portal hypertension.
 Bleeding peptic ulcers in view of Vomiting blood and abdominal pain
Examination:
General; noted a fairly looking young adult lying supine in bed with a canula insitu, afebrile to
touch with a temperature of 36.4C° with jaundice, conjunctival pallor, no central cyanosis, no
lymphadenopathy, no finger clubbing, no edema, no dehydration.
Per abdomen: On inspection, the abdomen was slightly distended but with normal symmetry
moving normally with respiration, no observable scars, no visible pulsations, no visible
collaterals and the umbilicus was everted. On superficial palpation; the abdomen was non
tender with no palpable subcutaneous mass. On deep palpation; a palpable mass in the left
upper quadrant which is non tender, smooth, moves with respiration infero-medially measuring
8cm. No any other palpable mass. A dull percussion note on the left upper quadrant and
resonate percussion notes in the other regions of the abdomen. On auscultation 5 bowel sounds
per minute normal in intensity and frequency.
C.V.S:pulse rate of 104b/min, normal rhythm, normal radial-radial syncrosity
but low volume B.P=130/56 mmHg, no engorged JV. Chest was warm, no
hyperactive pericardium, apex beat in 5th intercostal space. On auscultations
heart sounds I and II were heard with no added sounds.
Respiratory: RR=18 b/min, on inspection no visible scars and chest
deformities, symmetrical chest movements on respiration. On palpation no
tenderness, centrally located trachea, no palpable mass, the percussion note
in chest is resonate. On auscultation, normal breath sounds, no wheezing and
crackling sounds.
C.N.S: GSC=15/15, pupil react to light normally, alert and conscious, muscle
tone is 5/5
Differential diagnosis:
 Portal hypertension with bleeding varices
 splenomegaly
 bleeding peptic ulcers.
Investigations:
 CBCT
 MRDT and blood film for malaria
 LFTs
 HIV test, sickle cell test, blood culture
 abdominal ultra sound scan
 Abdominal CT scan
 H-pylori
 Endoscopy
 ANATOMY
GROSSLY (macroscopic anatomy)
The spleen is a firm organ of a dull red color, roughly the size and shape of a clenched fist (i.e.
ovoid).
Has 4 borders (anterior (notched), superior (may be notched), posterior and inferior (both which
are smooth) and 2 surfaces (diaphragmatic and visceral).
Its intraperitoneal suspended by the greater omentum ligaments i.e.;
gastrosplenic ligament (carrying the short gastric and left gastroepiploic vessels).
splenicorenal (lienorenal) ligament (carrying the splenic vessels and the tail of the pancreas).
Phrenicocolic ligament

The odd numbers 1, 3, 5, 7, 9, 11 summarize certain statistical features of the spleen i.e.
Has dimensions; 1X3X5 Inches = thicknessXwidithXlength.
weighs 7 ounces
It extends from the level of the 9th to the 11th ribs. (its long axis parallel to the shaft of the 10th rib
and does go beyond the mid axillary line thus cannot be palpated on clinical examination.)
Relations
 -Anteriorly, the stomach
 -Posteriorly, the left part of the diaphragm, which separates it from the pleura,
lung, and ribs 9–11
-Inferiorly, the left colic flexure
-Medially, the left kidney.

Neurovasculature (mainly through the hilum);

 Blood Supply
Arteries; splenic artery, the largest branch of the celiac artery; could arise from
aorta or superior mesenteruc artery
Veins; splenic vein which joins the superior mesenteric vein to form the portal
vein.
 Lymph Drainage; celiac nodes via lymphatics along the splenic artery.
 Nerve Supply; Para arterial (splenic artery) nervous plexus spleen is from the
coeliac plexus with sympathetic fibers only.
HISTOLOGICAL (MICROSCOPIC ANATOMY)
 The spleen Is surrounded by a capsule made up of dense connective
tissue and is covered in turn by the visceral peritoneum.
 Trabeculae extend inward from the capsule. The capsule plus
trabeculae, reticular fibers, and fibroblasts constitute the stroma of
the spleen; the parenchyma of the spleen consists of two different
kinds of tissue;
(1) White pulp; lymphatic tissue, consisting mostly of lymphocytes and
macrophages arranged around branches of the splenic artery called
central arteries.
(2) The red pulp consists of blood-filled venous sinuses and cords of
splenic tissue called splenic (Billroth’s) cords which consist of red
blood cells, macrophages, lymphocytes, plasma cells, and
granulocytes. Veins are closely associated with the red pulp.
Functions of the spleen
White pulp.
B cells and T cells carry out immune functions e.g. synthesis of antibodies by
T-cells and recognizing non-self antigens by T-cells, similar to lymph nodes,
while spleen macrophages destroy blood-borne pathogens by phagocytosis.
Examples of immune functions include IgM synthesis, formation of
lymphocytes, production of tuftsin, opsonins, properdins and interferons.
Red pulp.
(1) removal by macrophages of ruptured, worn out, or defective blood cells
and platelets; culling and pitting.
(2) Blood reservoir (up to 100 mL) and blood components platelets in
particular (up to one-third of the body’s supply); and
(3) production of blood cells (hematopoiesis) during fetal life or cases of
extra medullary hematopiesis.
Splenomegaly.
Enlargement of the spleen measured by weight and size. The spleen must be
enlarged to about 2-3 times for it to be palpable. Either below or underneath
the costal margin. Enlargement is first superoposteriorly and then
inferomedially, towards the iliac fossa
can be classified using Hackett’s Grading:
 Grade 0; Spleen not palpable
 Grade 1; Spleen palpable just below lower costal margin on deep inspiration.
 Grade 2; Spleen palpable <halfway between costal margin and umbilicus.
 Grade 3; Spleen palpable >halfway to the umbilicus but not beyond it.
 Grade 4; Spleen palpable below the umbilicus , but not beyond the line midway
between the umbilicus and pubic sympysis.
 Grade 5; Lower than in Grade 4.
Furthermore splenomegaly can be classified as:
 Massive splenomegaly( weight more than 1000g or extension >
8cm below the costal margin.
 Moderate splenomegaly ( weight 500- 1000g)
 Mild splenomegaly (weight less than 500g )
AETIOLOGY
Infectious splenomegaly
 Bacterial; infective endocarditis, septicemia,TB , streptococci,
staphylococci, cat-scratch disease, brucellosis, tularemia, plague,
chancroid, atypical mycobacterial infection, primary and secondary
syphilis, diphtheria and leprosy.
 Splenic filtering especially of encapsulated organisms may lead to
abscess formation
 Viral; EBV, CMV.
 Fungal; Histoplasmosis, coccidioidomycosis, paracoccidioidomycosis,
 Parasitic; plasmodium, leishmania, trypanosomiasis and hydatid disease.
 Splenic enlargement due to work hypertrophy, abscess formation. B.
 ……….AETIOLOGY

 Congestive splenomegaly
Hepatic causes
Liver cirrhosis, hepatic vein occlusion
Extrahepatic causes; Biliary atresia, cystic fibrosis, splenic vein occlusion by
emboli, portal hypertension, portal vein obstruction and sclerosing cholangitis.
Cardiac causes; congestive heart failure,
 Pathophysiology
 Phagocytosis of abnormal red blood cells
 Proliferation of splenic tissue particular the plasma cells as a result of antigenic
stimulation leading to antibody production.
 Portal hypertension
 Space occupying lesions with splenic capsule ( usually an abscess)
 Congestion (erythrostasis) in the red pulp of the spleen
 Extramedullary erythropoiesis
 Hyperplasia of mononuclear phagocytes
 To take note on examination…
Percussion

Nixon’s method
Percussion starts midway along left costal margin and is continued upward
perpendicular to the left costal margin. Normally dullness does not extend
further than 8 cm above the costal margin.
Percussion of the Traube’s space (Barkun’s method).
sixth rib superiorly, midaxillary line laterally and left costal margin inferiorly.
Normally the percussion note is resonant. dullness implies splenomegaly
Castell’s method
With the patient in a supine position, percuss the area of the lowest intercostal
space (8th -9th ) in the left anterior axillary line. If the note changes from the
resonant on full expiration to dull on full inspiration, the sign is regarded as
positive.
Management
 Splenectomy; usually used for management of symptoms; was in
the past used for staging
 Treatment of the underlying. cause e.g. antibiotics, chemotherapy,
radiotherapy.
 Management of symptoms like managing cytopenias by transfusion
Complications
 Infection and abscess formation
 Ruptured spleen which may lead to splenic tissue elsewhere causing
hypersplenism even after splenectomy
 Anaemia due to continued and massive red cell destruction.
 Severepost-splenectomy infection (usually H. influenza, streptococci and N.
meningitidis).
 Massive splenomegaly may result into intestinal obstruction.

References
Hutchison’s Clinical methods
Davidson’s principles and practices of medicine
Harrison's principles of internal medicine
Last’s Anatomy
 Thank you!

@ DE ARCK IZO