Category Archives: Surgery

What causes intestinal adhesions?

Intestinal adhesions can be caused by abdominal surgery, intraperitoneal infection, abdominal trauma, abdominal radiotherapy, congenital factors, etc., and can be relieved by medication or surgery. Prompt medical attention is recommended so that an appropriate treatment plan can be chosen under a doctor’s guidance.

Abdominal surgery
Abdominal surgery is the most common cause. Surgical manipulation may injure the bowel or peritoneum, triggering a local inflammatory reaction and fibrous tissue overgrowth. Appendectomy, hysterectomy, and other abdominal procedures carry a high risk. Patients may complain of abdominal pain, distension, or altered bowel habits. Amoxicillin capsules or cefixime dispersible tablets are often prescribed to prevent infection; severe cases may require adhesiolysis.
Intraperitoneal infection
Infections such as peritonitis or pelvic inflammatory disease produce hyperemic, edematous peritoneum; after the inflammation subsides, fibrous adhesions remain. Tuberculous peritonitis is particularly prone to extensive adhesions. Fever and abdominal tenderness are common. Therapy targets the primary infection with antibiotics such as levofloxacin or metronidazole; surgical drainage is sometimes necessary.
Abdominal trauma
Blunt or crush injuries can damage bowel or peritoneum, and adhesions form during healing. High-speed collisions or falls carry the greatest risk. Persistent pain and diminished bowel sounds may appear. Early symptoms can be controlled with ibuprofen sustained-release capsules; complete obstruction mandates surgery.
Abdominal radiotherapy
Radiation for pelvic or abdominal tumors may injure the serosal layer of the bowel, leading to chronic inflammation and fibrosis. Gynecologic or rectal cancers are the most frequent settings. Radiation enteritis with secondary adhesions presents as diarrhea or tenesmus. Doctors may prescribe montmorillonite powder or live combined Bifidobacterium capsules; severe cases can require a diverting stoma.
Congenital factors
A minority of patients have congenital maldevelopment of the mesentery or peritoneal defects that predispose to spontaneous adhesions. Intestinal malrotation is the classic example. Infants may present with recurrent pain or vomiting. Imaging confirms the diagnosis, and corrective surgery is performed when indicated.

Daily care
Patients should eat soft, low-fiber foods in small, frequent meals and avoid binge eating. Gentle abdominal massage and light exercise promote peristalsis, but strenuous activity should be avoided. Maintain regular bowel habits. Seek immediate care if pain worsens, vomiting develops, or flatus and stool cease—signs of possible obstruction. Postoperative patients must follow prescribed rehabilitation programs and attend scheduled follow-ups to monitor for recurrent adhesions.

No.	Cause	Mechanism / Typical settings	Common symptoms / signs	Medical treatment	Surgical treatment	Special notes
1	Abdominal surgery (most common)	Surgical trauma → local inflammation → fibrous overgrowth (e.g. after appendectomy, hysterectomy)	Abdominal pain, distension, altered bowel habits	Amoxicillin, cefixime (infection prophylaxis)	Adhesiolysis for severe obstruction	Highest incidence within first post-operative year
2	Intraperitoneal infection	Peritonitis, PID, TB peritonitis → exudative inflammation → fibrous adhesions after resolution	Fever, abdominal tenderness, leukocytosis	Levofloxacin, metronidazole; anti-TB drugs if indicated	Percutaneous or open drainage of abscess / dense adhesions	TB peritonitis tends to produce dense, wide-spread adhesions
3	Abdominal trauma	Blunt or crush injury (MVC, falls) → serosal tears → healing with adhesion formation	Persistent pain, diminished bowel sounds, signs of ileus	Ibuprofen SR (symptom relief), IV fluids	Laparotomy if complete obstruction or strangulation	High index of suspicion after high-energy trauma
4	Abdominal radiotherapy	Radiation-induced serositis → chronic inflammation & fibrosis (gynae/rectal cancers)	Diarrhea, tenesmus, bleeding, chronic pain	Montmorillonite powder, Bifidobacterium triple-therapy capsules	Diverting stoma or resection for refractory stricture	Dose-dependent; may present months to years after RT
5	Congenital factors	Maldevelopment of mesentery or peritoneal fixation defects (e.g. intestinal malrotation)	Neonatal/infantile recurrent pain, vomiting, failure to thrive	Supportive (NG decompression, fluids)	Corrective surgery (Ladd procedure, adhesiolysis)	Diagnose with upper-GI contrast series or US
Daily care for all patients	—	—	—	Low-fiber, easily digested diet; small frequent meals; gentle abdominal massage & light exercise; prompt medical review if pain ↑, vomiting, or no flatus/stool	—	Avoid strenuous activity; maintain regular bowel habits; scheduled follow-up for post-operative patients

What causes stone disease?

What Causes Stone Disease and How to Prevent It

Stones are usually caused by irregular lifestyle habits, a diet high in greasy and heavy foods, and genetic factors.

I. Causes of Stones

Diet – Consuming too many greasy and rich foods can lead to stone formation.
Lifestyle habits – Skipping breakfast, for example, affects gallbladder function. After eating at night, the gallbladder contracts once. If no food is eaten until late the next morning, the gallbladder remains full for up to 11 hours. This stagnant bile in a distended gallbladder can easily form gallstones.
Hormonal factors – Women tend to have higher estrogen levels, which can increase cholesterol saturation in bile and reduce gallbladder tone, promoting cholesterol deposition and gallstone formation.
Genetics – Some families have a higher predisposition to gallstones, indicating a genetic component. Thus, stones can have a hereditary aspect.

II. Prevention of Stones

Drink plenty of water and avoid holding urine – This helps flush out stone-forming substances and bacteria from the urinary tract.
Limit beer consumption – Beer contains high levels of calcium, oxalate, and purines. Excessive intake can promote the deposition of stone-forming substances in the urinary system.
Reduce intake of high-protein and high-fat foods – Limit consumption of meat and animal organs. Excessive intake can disrupt purine metabolism, increase uric acid levels, and lead to urinary stones.
Avoid excessive salt – Salty foods burden the kidneys and impair metabolism, causing stone-forming substances to accumulate in the kidneys and body.
Be cautious with spinach – Spinach is rich in oxalic acid, a key component in the formation of oxalate urinary stones.

In summary, stone formation is closely related to lifestyle and diet. It is recommended to drink plenty of water, exercise regularly, undergo routine check-ups, and seek early treatment if stones are detected.

Section	Item	Details
Causes	1. Diet	Excessive greasy / heavy foods promote stone formation.
	2. Lifestyle	Skipping breakfast → gallbladder remains distended ≥ 11 h → bile stasis → gallstones.
	3. Hormones	High estrogen (esp. women) ↑ cholesterol saturation & ↓ gallbladder tone → gallstones.
	4. Genetics	Family history / gene variants ↑ risk of gallstones.
Prevention	1. Hydration	Drink plenty of water; do not delay urination—flushes stone-forming substances & bacteria.
	2. Alcohol	Limit beer (rich in Ca²⁺, oxalate, purines) to reduce urinary deposition.
	3. Diet macro	Cut high-protein & high-fat foods; restrict meat / organ meats to control purine → uric-acid stones.
	4. Salt	Lower salt intake to lessen renal load and solute accumulation.
	5. Oxalate	Consume spinach cautiously (high oxalate → oxalate stones).
Summary	—	Stones link to diet & lifestyle. Advised: drink water, exercise, regular check-ups, treat early.

peritoneal thickening

In general, peritoneal thickening is most often caused by abdominal trauma, peritonitis, or metastatic malignancy. Prompt evaluation with contrast-enhanced abdominal CT or PET-CT is essential to establish the exact aetiology; treatment may then include drugs, radiotherapy, chemotherapy, or surgery.

Abdominal trauma
A direct blow can produce local oedema or haematoma that widens the peritoneal stripe. After imaging to define the extent, small haematomas are managed conservatively, but a full-thickness peritoneal tear requires surgical repair.
Peritonitis
Bacterial infection, hollow-viscus perforation, or intraperitoneal bleeding can incite marked peritoneal inflammation and subsequent thickening, classically presenting with nausea, vomiting and abdominal pain. Intravenous antibiotics (e.g. ceftriaxone, cefoperazone–sulbactam) are given to control sepsis; laparoscopic lavage or definitive repair is undertaken when indicated.
Malignant peritoneal metastasis
Advanced gastric, colonic or ovarian cancers may seed the peritoneum, producing plaque-like thickening. Curative resection is seldom possible; cytoreductive surgery is considered only after a good response to systemic chemotherapy or palliative radiotherapy.

Patients should adopt a light, easily digested diet, avoid cold, greasy or irritating foods, and ensure adequate rest and warmth while the diagnostic and therapeutic plan is completed.

Cause	Mechanism / Key Points	Diagnostic Note	Treatment & Nursing
Abdominal trauma	Direct blow → local oedema / haematoma → peritoneal stripe widens	CT to size haematoma / detect tear	Small: conservative; Peritoneal tear: surgical repair
Peritonitis	Bacterial infection, perforation, intraperitoneal bleed → inflammation & thickening; presents with nausea, vomiting, abdominal pain	CT ± paracentesis; sepsis work-up	IV antibiotics (ceftriaxone, cefoperazone-sulbactam); laparoscopic lavage / repair if needed
Malignant metastasis	Gastric, colonic, ovarian etc. seeds peritoneum → plaque-like thickening	CT + tumour markers; PET-CT for extent	Systemic chemotherapy ± palliative RT; cytoreductive surgery only if good response
General supportive care	—	—	Light, easily digested diet; avoid cold, greasy foods; adequate rest & warmth

Should patients with kidney stones take calcium supplements?

Calcium is an essential mineral that accounts for 1.5–2 % of total body weight; an average adult therefore carries ≥ 1 200 g. Roughly 99 % is locked in bone and teeth, while 1 % circulates in blood, maintaining a dynamic equilibrium with the skeletal reservoir. Insufficient calcium causes growth retardation, osteoporosis, joint pain and muscular weakness. Modern nutrition holds that calcium should be supplied throughout life, especially for children, the elderly, post-menopausal women—and even stone-formers.

Nephrolithiasis is common after middle age. The traditional view that “high calcium intake begets stones” has been questioned. Ninety percent of renal calculi are calcium oxalate, yet结石 formation is now viewed as the net result of multiple factors: genetics, endocrine status, co-morbidities, obesity, parasites, food preferences and serum calcium. Four principal mechanisms are recognised: supersaturation, inhibitory activity, promotor activity and crystal retention. A large British trial found that subjects with the highest calcium intake had the lowest stone incidence. The real culprit is not dietary calcium but disordered calcium metabolism. When bone calcium is mobilised to blood, vascular smooth muscle contracts, small vessels spasm and “senile” hypertension may follow. In the kidney, oxalate concentration—not calcium load—drives crystallisation. If oxalate is abundant it will bind calcium released from bone and form new stones or enlarge existing ones even when calcium intake is zero. Restriction therefore offers no protection, whereas rational calcium supplementation is safe and necessary; otherwise the elderly lose bone mass and develop more severe osteoporosis.

Dietary calcium is the preferred source. Stone patients are encouraged to eat tofu, milk, yoghurt, small fish eaten with bone, shrimp shells and marine products—foods that supply protein along with easily absorbed, loosely structured calcium that resists crystallisation. Simultaneously, reduce high-oxalate items and exploit anionic competition: drink citrus-based beverages or eat fruit to provide citrate, which competes with oxalate for free calcium and limits insoluble calcium-oxalate deposition.

When dietary measures are insufficient, add a bio-active calcium preparation (pearl calcium, Ju-neng-calcium, Caltrate-D, Shen-yi active calcium powder) plus vitamin D to enhance intestinal uptake. Calcium gluconate and plain calcium carbonate are poorly utilised. The anion of bio-active calcium binds excess cations (Ca²⁺, Mg²⁺) in the renal tubule and carries them out as insoluble salts. Absorption also requires phosphorus in a Ca:P ratio of 3:2; milk, eggs, meat, fish and legumes supply phosphorus. A daily intake of 1–1.5 g calcium neither exacerbates stones nor harms kidneys and will improve osteoporosis. Intakes > 2 g may precipitate in the kidney. Alcohol and coffee should be limited during supplementation.

Finally, existing calculi should be removed when indicated, and prevention continued:

Drink enough water to lower urinary supersaturation and wash out calcium oxalate crystals.
Avoid or blanch high-oxalate foods (spinach, strawberry, amaranth, water-spinach stem, beet, black tea, chocolate, dried bamboo shoot, pickled vegetables).
Pharmacological inhibitors—magnesium, potassium citrate, orthophosphate, exogenous acid mucopolysaccharides—further reduce stone recurrence.

Section	Key Messages (English)
Body calcium facts	1.5–2 % of body wt (≈ 1 200 g); 99 % in bone/teeth, 1 % in blood; deficiency → growth failure, osteoporosis, pain, weakness.
Lifelong needs	Children, elderly, post-menopausal women & stone-formers must maintain intake.
Old vs new theory	Excess Ca NOT the cause; disordered Ca metabolism mobilises bone Ca → high serum Ca & oxalate still crystallises if urinary oxalate high.
Evidence	Large UK study: higher Ca intake → lower stone risk; restriction does NOT prevent stones but promotes osteoporosis.
Preferred source	Diet first: tofu, dairy, small fish with bones, shrimp, marine products (high absorption, low crystallisation risk).
Anti-oxalate tactics	Limit high-oxalate foods; use citrate (citrus drinks/fruit) to compete with oxalate for Ca.
Supplement if needed	Bio-active Ca (pearl Ca, Caltrate-D, etc.) + vitamin D; avoid poor-absorption salts (gluconate, plain carbonate).
Ca:P ratio	Maintain 3:2 with phosphorus-rich foods (milk, eggs, meat, fish, legumes).
Safe dose	1–1.5 g/day: improves bone, does NOT worsen stones; > 2 g/day may precipitate in kidney.
Lifestyle during Rx	Avoid alcohol & coffee; stay well-hydrated.
General prevention	Drink plenty of water; blanch high-oxalate veg; consider inhibitors (Mg, K-citrate, orthophosphate, acid mucopolysaccharides).

How are gastrointestinal bezoars diagnosed?

Gastrointestinal bezoars are a common condition both in daily life and in clinical practice. They arise when a person eats foods that readily form concretions; the resulting signs vary with the size and consistency of the mass. Careful, step-by-step evaluation is therefore essential to avoid misdiagnosis or delayed diagnosis and the added morbidity these errors entail.

Diagnostic work-up

History
Recent intake of persimmon, hawthorn, or black jujube followed by epigastric pain, repeated vomiting, or melena should raise immediate suspicion. Confirmation is obtained endoscopically and/or radiologically.

Laboratory tests

Microcytic hypochromic anaemia in some patients
Positive faecal occult blood; early stools may contain persimmon-skin-like debris
Gastric acid analysis: free acid often higher than normal

Imaging & endoscopy

X-ray (barium meal or double-contrast)
– Barium stream is diverted; a free-floating, round/oval filling defect is seen on top of the barium pool.
– Mucosal pattern is intact and the wall remains pliable.
– After gastric emptying, streaky, reticular or patchy barium still clings to the mass, which changes shape and position when compressed, indicating compressibility and mobility.
Gastro-duodenoscopy (first-line procedure)
– Directly visualises colour (yellow, brown, green, black) and shape (single or multiple spheres, “J”-shaped or kidney-shaped).
– Phytobezoars are usually yellow-brown; trichobezoars are black/dark-brown and may extend into the duodenum.
– Permits biopsy of bezoar fragments and of any accompanying gastritis or ulcer.
Ultrasonography
– After 500–1000 mL water, a well-demarcated strongly echogenic mass is seen floating in the fluid layer and shifting with posture or peristalsis.

Differential diagnosis

Functional dyspepsia – dyspeptic symptoms but negative endoscopy/barium study.
Chronic gastritis – irregular upper-abdominal pain; endoscopy shows chronic antral changes.
Zollinger–Ellison (gastrinoma) – BAO > 15 mmol/h, BAO/MAO > 0.6, atypical/multiple refractory ulcers, diarrhoea, serum gastrin > 200 pg/ml (often > 500).
Malignant gastric ulcer/gastric cancer – excluded by endoscopy with biopsy and barium study.
Prolapse of gastric mucosa – intermittent pain unrelieved by antacids but eased by left lateral decubitus; barium may show a “mushroom” or “parachute” defect in the duodenal bulb.

Because bezoars can masquerade under many guises, active prevention is vital: regular exercise, balanced meals, careful eating habits and avoidance of foods known to precipitate concretions will minimise the risk and keep the gastrointestinal tract clear.

Category	Key points (English)
Clinical suspicion	Recent persimmon / hawthorn / black-jujube intake + epigastric pain, vomiting, melena.
Laboratory tests	Microcytic anaemia; + faecal occult blood; persimmon-skin debris; ↑ gastric free acid.
X-ray barium study	Free-floating round/oval filling defect on barium pool; mucosa intact; mass compressible & mobile; residual barium clings after emptying.
Endoscopy (1st-line)	Direct view of colour/shape; distinguishes phytobezoar vs trichobezoar; allows biopsy; detects gastritis / ulcer.
Ultrasonography	After 500–1000 mL water: strongly echogenic mass floating in gastric fluid, shifts with posture/peristalsis.
Differential diagnoses	1. Functional dyspepsia – symptoms only, negative imaging. 2. Chronic gastritis – endoscopy shows antral changes. 3. Zollinger–Ellison – high BAO, multiple atypical ulcers, ↑ serum gastrin. 4. Malignancy – ruled out by endoscopy + biopsy. 5. Gastric mucosal prolapse – intermittent pain, “mushroom” defect on barium.
Prevention advice	Regular exercise; balanced low-oxalate, high-fiber diet; chew food thoroughly; limit bezoar-promoting fruits (persimmon, hawthorn, etc.).

What dietary precautions should be taken for gastrointestinal stones?

Gastrointestinal stones (bezoars) are a serious condition that can greatly affect a patient’s health. The points below summarize the main dietary measures doctors usually recommend after surgery so that new stones do not form.

Drink plenty of plain water every day
A high fluid intake dilutes the intestinal and urinary contents, lowering the concentration of calcium and oxalate and reducing the risk of recurrent stones.
Add black fungus (wood-ear mushroom, Auricularia) to the diet when permitted
This food is rich in minerals and dietary fiber; it is traditionally thought to “soften” and break up debris so that fragments can be swept out of the gut.
Replace calcium correctly if a supplement is needed
Do NOT stop calcium suddenly—ask the surgeon or dietitian when and how much to take, and whether it should come from dairy, fortified foods, or a tablet.
Make sure vitamin A is adequate, but never excessive
Vitamin A keeps the mucous lining of the GI and urinary tracts healthy and may help prevent crystal adhesion. Foods such as broccoli, apricot, cantaloupe, pumpkin, and beef liver are good sources, but high-dose pills can be toxic, so always confirm the dose with your doctor.
Keep a balanced, low-oxalate, moderate-fat, high-fiber diet
Avoid large amounts of spinach, rhubarb, beet, cocoa, strong tea, and very salty or very fatty snacks. Eat regular small meals and chew food thoroughly to reduce the chance of new bezoar formation.

By following these simple rules and returning for regular check-ups, most patients can keep their digestive system free of stones and avoid further trouble.

Post-operative dietary care for gastrointestinal stones (bezoars)	Key recommendations
1. Fluid intake	Drink plenty of plain water daily to dilute gut/urine content ↓ calcium & oxalate concentration.
2. Functional food	Include black fungus (wood-ear mushroom) – traditional fiber-rich food believed to soften & dislodge debris.
3. Calcium balance	Resume/supplement calcium only as directed by doctor; avoid both deficiency and excess.
4. Vitamin A	Maintain adequate intake (broccoli, apricot, cantaloupe, pumpkin, beef liver) to support mucosal health; high-dose supplements toxic—check dose first.
5. General diet	Low-oxalate, moderate-fat, high-fiber meals; limit spinach, rhubarb, beet, cocoa, strong tea, salty/fatty snacks; chew food well & eat small regular meals to prevent recurrence.

How is extracorporeal shock wave lithotripsy (ESWL)?

Extracorporeal shock-wave lithotripsy (ESWL) was introduced into clinical practice in the early 1980s. Experience has shown it to be a safe, effective and non-invasive treatment; the majority of upper-urinary-tract stones can be managed in this way.

Success depends not only on stone size but also on location, chemical composition and anatomical factors.

Stone size: Renal stones < 20 mm in diameter should be considered first-line for ESWL.
Stone location: Pelvic stones fragment most readily; upper- and mid-calyceal stones respond better than lower-pole stones.
Stone composition: Struvite and calcium-oxalate-dihydrate stones break easily; uric-acid stones can be treated with ESWL combined with dissolution therapy; calcium-oxalate-monohydrate and cystine stones are hard and more difficult to fragment.
Anatomical anomalies: Horseshoe, ectopic or transplant kidneys and congenital collecting-system deformities may impair fragment clearance; ancillary measures to assist passage can be employed.

Treatment sessions and intervals: No more than 3–5 ESWL sessions are recommended (exact number depends on the lithotripter used). No uniform interval is mandated, but most investigators, considering the time required for renal recovery after injury, advise 10–14 days between sessions.

Current contraindications: pregnancy, uncorrected bleeding diathesis, obstruction distal to the stone, severe obesity or skeletal deformity, and high-risk conditions such as heart failure, serious cardiac arrhythmia, or active genitourinary tuberculosis.

Topic	Key Points
Introduction	Introduced early 1980s; safe, non-invasive first-line for most upper-tract stones.
Stone size	< 20 mm renal stones = ideal candidates.
Stone location	Pelvic > upper/mid-calyx > lower-pole efficacy.
Stone composition	Easy: struvite, Ca-oxalate-dihydrate; Uric acid: ESWL + dissolution; Hard: Ca-oxalate-monohydrate, cystine.
Anatomical anomalies	Horseshoe, ectopic, transplant kidney or collecting-system deformity may hinder clearance → ancillary aids.
Session limit	≤ 3–5 treatments (device-dependent).
Interval between sessions	Advisable 10–14 days to allow renal recovery.
Contra-indications	Pregnancy, uncorrected bleeding, distal obstruction, severe obesity/skeletal deformity, heart failure, serious arrhythmia, active UGTB.

Why does lithotripsy hurt or not hurt?

Anesthesia is given during lithotripsy, so pain is usually minimal; however, colicky pain may appear later when stone fragments pass down the ureter. Therefore some discomfort is possible during the whole stone-removal process.

Main lithotripsy techniques:

Extracorporeal shock-wave lithotripsy (ESWL)
- Suitable for renal stones ≤ 2 cm
- Stones are localized by X-ray or ultrasound and fractured with focused high-energy shock waves; the resulting sand-like particles are voided with urine.
Ureteroscopic lithotripsy / stone extraction
- Rigid or flexible scopes (flexible scopes preferred for renal pelvis or calyceal stones)
- Used for radiolucent or ESWL-resistant stones < 2 cm; the scope is passed retrograde up to the renal collecting system, stones are fragmented and removed.
Percutaneous nephrolithotomy (PCNL)
- Recommended for stones > 2 cm
- Under X-ray or ultrasound guidance a needle tract is created from the skin through the renal cortex; nephroscopy is performed and stones are broken (ultrasonic, laser or pneumatic) and extracted.

In summary, although some pain can occur, it is generally tolerable. After any of these procedures generous fluid intake and frequent voiding are essential to help clear the fragments.

Aspect	Key Points
Intra-operative pain	Anesthesia provided; pain usually minimal.
Post-operative pain	Ureteral spasm may occur while fragments pass → colicky pain; generally tolerable.
ESWL ≤ 2 cm	X-ray/US localization; shock waves pulverize stone to sand, voided with urine.
Ureteroscopy < 2 cm	Flexible/rigid scope retrograde; fragment & extract radiolucent or ESWL-resistant stones.
PCNL > 2 cm	Percutaneous tract; nephroscopic ultrasonic/laser/pneumatic fragmentation & extraction.
Universal after-care	High fluid intake + frequent voiding to flush out fragments.

How long does it take for the stone fragments to pass after extracorporeal shock-wave lithotripsy (ESWL)?

After extracorporeal shock-wave lithotripsy (ESWL), the time needed for stone expulsion depends on the size and hardness of the fragments. In most cases, passage begins only after one day; soft stones may be expelled on the same day.

Although ESWL can break the stone into pieces, these pieces are still discrete fragments. They have to be flushed out by drinking plenty of water and urinating frequently. The recommended fluid intake is 2 000–3 000 mL per day. Patients are also advised to walk around so that the fragments can migrate and be expelled more easily. A small portion of the fragments starts to come out one day after the procedure, and the bulk of the material is then passed gradually; in general, the majority of fragments clear within one day. Large or hard stones may not be completely disintegrated by a single session; a second lithotripsy one week later may be required, and only after the stone is reduced to fine gravel can complete expulsion occur.

During the passage period, mild abdominal pain and sometimes haematuria are normal; increasing fluid intake is usually sufficient.

Item	Details
Onset of expulsion	Usually begins ≥ 1 day after ESWL; soft stones may pass same day.
Mechanism	Fragments are flushed by high fluid intake (2–3 L/day) and physical activity (walking).
Time-course	First fragments appear after 24 h; majority clear within 1 day if complete fragmentation achieved.
Hard/large stones	May require a second session 1 week later; only after further breaking can all fragments pass.
Expected symptoms	Mild abdominal pain, transient haematuria; managed by increased oral fluids.

How many days of rest are needed after extracorporeal shock-wave lithotripsy (ESWL)?

Patients should rest for at least three days after extracorporeal shock-wave lithotripsy (ESWL); the exact period is adjusted according to how smoothly the stone fragments pass.

The repeated shock waves produce mild trauma to the kidney or ureter, leading to localized edema and sometimes small mucosal tears. This explains the slight abdominal pain or discomfort commonly felt after the procedure. Provided the symptoms are tolerable, no extra intervention is required.

Post-ESWL routine

Drink plenty of water
Perform gentle activity (walking) to help gravel descend
Avoid strenuous exercise, which can intensify pain while edema is present

Minimum 3-day rest is advised. On the third day, if pain and hematuria have resolved, the patient returns for imaging:

No residual fragments → resume normal work and life
Residual stones → second lithotripsy session and a longer rest period

Additional advice: stay relaxed, and refrain from spicy or irritating foods.

Item	Instructions / Time-frame
Minimum rest	3 days
Why rest?	Renal/ureteral edema or small mucosal tears caused by shock waves
Allowed activities	Plenty of water, gentle walking to help fragments pass
Forbidden	Strenuous exercise (worsens pain & edema)
Review on day 3	Imaging check:
• No residual stones	Resume normal activity
• Residual stones	Second ESWL → longer rest
Diet & mood	Stay relaxed; avoid spicy / irritating foods

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Category Archives: Surgery

What causes intestinal adhesions?

What causes stone disease?

peritoneal thickening

Should patients with kidney stones take calcium supplements?

How are gastrointestinal bezoars diagnosed?

What dietary precautions should be taken for gastrointestinal stones?

How is extracorporeal shock wave lithotripsy (ESWL)?

Why does lithotripsy hurt or not hurt?

How long does it take for the stone fragments to pass after extracorporeal shock-wave lithotripsy (ESWL)?

How many days of rest are needed after extracorporeal shock-wave lithotripsy (ESWL)?

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