Definition of Diagnosis

The final diagnosis of the patient would be Acute Cholecystitis secondary to

Cholelithiasis. According to Tokyo Guidelines diagnostic criteria for acute cholecystitis
that there are 3 categories: (A) Local signs of inflammation etc. which includes Murphy’s
sign, or RUQ mass/pain/tenderness; (B) Systemic signs of inflammation etc. which
includes fever, elevated CRP, or elevated WBC count; and (C) Imaging findings which
has characteristic of acute cholecystitis. A definite diagnosis of acute cholecystitis would
be 1 item in A (RUQ pain) + 1 item in B (elevated WBC count) + C (positive findings
characteristics of acute cholecystitis due to gallbladder stone/cholelithiasis) (Takada,
2018).
As much as 90% to 95% of the cases of acute cholecystitis is responsible for
gallstone-associated cystic duct obstruction (Gallaher and Charles, 2022). Acute
cholecystitis is usually caused by obstruction of gallbladder neck or cystic duct by stone
impacted on the cystic duct. A possible need for cholecystectomy for cholelithiasis
which is a common disease of the biliary tract which can result in cholecystitis
(Anderson et al., 2019).

Anatomy and Physiology

Anatomy
The gallbladder is a sac with a pear-like shape that ranges in size from 7 to 10
cm long with a 30 to 50 mL capacity on average. It can distend markedly and contain up
to 300mL when obstructed. It is located in an anatomic fossa on the liver's inferior
surface. Cantle's line which is a vertical plane running from the gallbladder fossa
anteriorly to the inferior vena cava (IVC) posteriorly divides the lover into right and left
lobes, The gallbladder is divided into 4 anatomical areas: fundus, body, infundibulum,
and neck. The left lobes. The gallbladder is separated anatomically into four parts. The
body mainly stores the bile, its body tapers towards the neck of the gallbladder and the
cystic duct (infundibulum or Hartmann’s pouch).
The same peritoneal lining that surrounds the liver extends to cover the fundus
and the inferior surface of the gallbladder. The mucosal lining is composed of smooth
muscle and fibrous tissue, its lumen is high columnar epithelium containing cholesterol
and fat globules. Its blood supply comes from cystic artery that supplies the gallbladder
is usually a branch of the right hepatic artery, and venous drainage comes from the
cystic vein and small vein coming from the gallbladder toward the liver. Lymph node
from gallbladder to the liver then to nodes along surface of portal vein. The nerve supply
arise from celiac plexus that lie along hepatic artery.
The extrahepatic biliary system starts from the right and left hepatic ducts which
are coming from the right lobe and the left lobe of the liver, respectively. Once they
converge together, they become the common hepatic duct. Then once this common
hepatic duct is joined by the cystic duct coming from the gallbladder, this now become
the common bile duct. The common bile duct extends distally towards the duodenum
where it drains the bile. This segment is typically about 7 to 11 cm in length and 5 to 10
mm in diameter. There are 3 portions of common bile duct namely: upper third
(supraduodenal portion), middle third (retroduodenal portion), and lower third
(pancreatic portion). The duct then runs obliquely downward within the wall of the
duodenum before opening on a papilla of mucous membrane (ampulla of Vater). The
sphincter of Oddi controls the flow of bile, and in some cases pancreatic juice, into the
duodenum. The extrahepatic bile ducts are lined by a columnar epithelium with many
mucous glands that are concentrated in the common bile duct. Its arterial supply is
derived from the gastroduodenal and the right hepatic arteries. The nerve supply is the
same as for the gallbladder (Anderson et al., 2019).

Physiology

The physiology of the gallbladder, biliary tree, and sphincter of Oddi are
regulated by a complex interplay of hormones and neuronal inputs designed to
coordinate bile release with food consumption. It is the liver that produces bile
continuously and excretes it into the bile canaliculi. The bile leaves the liver thru the
right and left hepatic ducts, into the common hepatic duct and then the common bile
duct. The sphincter of Oddi which contracts and diverts the flow of the bile into the
gallbladder for storage. The normal adult consuming an average diet produces 500 to
1000 mL of bile a day. The secretion of bile is responsive to neurogenic, hormonal, and
chemical stimuli. After a meal, the hydrochloric acid, partly digested proteins, and fatty
acids entering the duodenum from the stomach will stimulate the release of secretin,
and increases production of bile and flow. Bile is mainly composed of water, mixed with
bile salts and acids, cholesterol, phospholipids (lecithin), proteins, and bilirubin. The
cholate and chenodeoxycholate which are primary bile salts, are synthesized in the liver
from cholesterol metabolism and are then excreted into the bile by hepatocytes and
helps in digestion and absorption of fats in the intestines.

The gallbladder, bile ducts, and the sphincter of Oddi act together to store and
regulate the flow of bile. The main function of the gallbladder is to concentrate and store
hepatic bile in order to deliver it in a coordinated fashion to the duodenum in response
to a meal. It rapidly absorbs sodium, chloride, and water which then concentrates the
bile as much as 10-fold and will result to a marked change in bile composition. The
gallbladder’s mucosal glands secrete at least two important products into the
gallbladder lumen: glycoproteins and hydrogen ions. These mucosal glands are
believed to protect the mucosa from the harmul action of bile and to facilitate the
passage of bile through the cystic duct. It is the transport of hydrogen ions that
decreases the pH of stored bile. This may cause acidification which helps to prevent the
precipitation of calcium salts, which can act as a nidus for stone formation.

Bile passage to duodenum involves gallbladder contraction & Sphincter of Oddi

relaxation. When you ingest food, there is a release of cholecystokinin (CKK) which
then contracts gallbladder wall, relaxes terminal bile duct, Sphincter of Oddi and
duodenum. Vagys nerve also stimulates the gallbladder contraction. Splanchnic
sympathetic stimulation inhibits motor activity of gallbladder. Gallbladder emptying takes
place 30 minutes after fatty meals and gallbladder filling occurs when bile duct pressure
is greater than that within the gallbladder which is correlated with low CCK levels,
vasoactive intestinal peptide, pancreatic peptide, and peptide YY. Gallstones form as a
result of solids settling out of solution and the major organic solutes in bile are bilirubin,
bile salts, phospholipids, and cholesterol (Anderson et al., 2019).

II. PATHOPHYSIOLOGY
A. Etiology
Table 1.1: Predisposing Factors of Acute Cholecystitis secondary to cholelithiasis
PREDISPOSING PRESENT RATIONALE
FACTORS

Age x There is an increased risk if the patient is 40 and

above years old (Antonio et al., 2018).

Sex x
Women are 3x more likely to develop gallstones
than men (Anderson et al., 2019).
 Fertile x
(Multiparity) Fertile women has higher risk (Antonio et al., 2018).

Ethnicity x Increased prevalence in patients of Native American

and Latin American descent (Anderson et al., 2019).

Family history x First-degree relatives of patients with gallstones

have a twofold greater prevalence, possibly
indicating a genetic predisposition (Anderson et al.,
2019).

Certain conditions x Some conditions predispose to the development of

gallstones including pregnancy, non-HDL
hyperlipidemia, Crohn’s disease, and certain blood
disorders such as hereditary spherocytosis, sickle
cell disease, and thalassemia (Anderson et al.,
2019).

Table 1.2: Precipitating Factors of Acute Cholecystitis secondary Cholelithiasis

PRECIPITATING PRESENT RATIONALE
FACTORS

Fat (obesity) x When there is presence of cholesterol

hypersecretion, either through increased intake or
dysfunctional processing, there is supersaturation
of the secreted bile forming a cholesterol stone
(Anderson et al., 2019).

Rapid weight loss x Due to bariatric surgery or lifestyle changes can

also precipitate gallstone formation by creating an
imbalance in bile composition (Anderson et al.,
2019).

Surgery x This can alter the normal neural or hormonal

regulation of the biliary tree including terminal ileal
resection and gastric or duodenal surgery increase
the risk of cholelithiasis (Anderson et al., 2019).

Medications x Somatostatin analogues and estrogen-containing

oral contraceptives are also associated with an
increased risk of developing gallstones (Anderson
et al., 2019).

High fat diet x About 80% of gallstones are cholesterol in Western

countries. The primary event in the formation of
cholesterol stones is supersaturation of bile with
 cholesterol.

B. Symptomatology
Table 2: Symptomatology
SYMPTOMS PRESENT RATIONALE

Presence of / Ultrasound has a high specificity as well sensitivity for

Stones in the cholelithiasis. The density of gallstone in ultrasound
Gallbladder shows an echogenic focus with a characteristic
shadowing behind the stone. There gallbladder wall
thickening and prericholecystic fluid seen in
cholecystitis (Townsend et al., 2022).

Right Upper / The pain develops due to a stone obstruction on the

Quadrant cystic duct which results in the distension of the
Abdominal Pain gallbladder wall as it contracts in response to a meal.
(Biliary Colic) In addition to pain, gallstones may progress to cause
complications such as acute cholecystitis (Anderson
et al., 2019).

Elevated White / An elevated white blood cell (WBC) count may

Blood Cell Count
indicate an infection within the gallbladder (acute
cholecystitis) (Anderson et al., 2019). Infection in the
absence of obstruction is rare through low bacteria
load and flow of bile but with gallstones or
obstruction, there is higher chance of increased
bacterial infection (Townsend et al., 2022).

Nausea and / The pain usually occur at night or after a fatty meal
Vomiting and it is severe and abrupt. This biliary colic is
associated with nausea and sometimes vomiting, and
these patients generally suffer discrete, recurrent
attacks of pain, between which they feel well
(Anderson et al., 2019).

Increased / High concentrations of cholesterol and lipid in bile

Cholesterol secretion from the liver may contribute to gallbladder
Production stone. These stones in the gallbladder are formed
due to supersaturation of secreted bile, concentration
of bile in the gallbladder, crystal nucleation, and
gallbladder dysmotility (Townsend et al., 2022).

Fever / There is an infection of the biliary tree (cholecystitis)

(Townsend et al., 2022).

Jaundice x This suggests and obstruction of the duct due to the

 stones. Hyperbilirubinemia may be secondary
increased direct bilirubin possibly due to obstruction
(Townsend et al., 2022).

Increased / Cholestasis which is an obstruction to bile flow is

Alkaline characterized by elevation in alkaline phosphatase,
Phosphatase but it may have no transaminitis (Anderson et al.,
2019).

References

Billiar, T., Brunicardi, F. C., Dunn, D., Andersen, D. K., Matthews, J., Hunter, J. G., &

Pollock, R. E. (2022). Schwartz's principles of surgery Absite and board

review (11th ed.). McGraw-Hill Education / Medical.

Takada, T. (2018). Tokyo guidelines 2018: Updated Tokyo guidelines for the

management of acute cholangitis/acute cholecystitis. Journal of Hepato-Biliary-

Pancreatic Sciences, 25(1), 1-2. https://doi.org/10.1002/jhbp.526

Townsend, C. M., Beauchamp, R. D., Evers, B. M., & Mattox, K. L. (2022). Sabiston

textbook of surgery: The biological basis of modern surgical practice (21st ed.).

Gallaher JR, Charles A. Acute Cholecystitis: A Review. JAMA. 2022;327(10):965–975.

doi:10.1001/jama.2022.2350