Category Archives: General 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.

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.CauseMechanism / Typical settingsCommon symptoms / signsMedical treatmentSurgical treatmentSpecial notes
1Abdominal surgery (most common)Surgical trauma → local inflammation → fibrous overgrowth (e.g. after appendectomy, hysterectomy)Abdominal pain, distension, altered bowel habitsAmoxicillin, cefixime (infection prophylaxis)Adhesiolysis for severe obstructionHighest incidence within first post-operative year
2Intraperitoneal infectionPeritonitis, PID, TB peritonitis → exudative inflammation → fibrous adhesions after resolutionFever, abdominal tenderness, leukocytosisLevofloxacin, metronidazole; anti-TB drugs if indicatedPercutaneous or open drainage of abscess / dense adhesionsTB peritonitis tends to produce dense, wide-spread adhesions
3Abdominal traumaBlunt or crush injury (MVC, falls) → serosal tears → healing with adhesion formationPersistent pain, diminished bowel sounds, signs of ileusIbuprofen SR (symptom relief), IV fluidsLaparotomy if complete obstruction or strangulationHigh index of suspicion after high-energy trauma
4Abdominal radiotherapyRadiation-induced serositis → chronic inflammation & fibrosis (gynae/rectal cancers)Diarrhea, tenesmus, bleeding, chronic painMontmorillonite powder, Bifidobacterium triple-therapy capsulesDiverting stoma or resection for refractory strictureDose-dependent; may present months to years after RT
5Congenital factorsMaldevelopment of mesentery or peritoneal fixation defects (e.g. intestinal malrotation)Neonatal/infantile recurrent pain, vomiting, failure to thriveSupportive (NG decompression, fluids)Corrective surgery (Ladd procedure, adhesiolysis)Diagnose with upper-GI contrast series or US
Daily care for all patientsLow-fiber, easily digested diet; small frequent meals; gentle abdominal massage & light exercise; prompt medical review if pain ↑, vomiting, or no flatus/stoolAvoid 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

  1. Diet – Consuming too many greasy and rich foods can lead to stone formation.
  2. 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.
  3. 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.
  4. Genetics – Some families have a higher predisposition to gallstones, indicating a genetic component. Thus, stones can have a hereditary aspect.

II. Prevention of Stones

  1. Drink plenty of water and avoid holding urine – This helps flush out stone-forming substances and bacteria from the urinary tract.
  2. 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.
  3. 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.
  4. Avoid excessive salt – Salty foods burden the kidneys and impair metabolism, causing stone-forming substances to accumulate in the kidneys and body.
  5. 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.

SectionItemDetails
Causes1. DietExcessive greasy / heavy foods promote stone formation.
2. LifestyleSkipping breakfast → gallbladder remains distended ≥ 11 h → bile stasis → gallstones.
3. HormonesHigh estrogen (esp. women) ↑ cholesterol saturation & ↓ gallbladder tone → gallstones.
4. GeneticsFamily history / gene variants ↑ risk of gallstones.
Prevention1. HydrationDrink plenty of water; do not delay urination—flushes stone-forming substances & bacteria.
2. AlcoholLimit beer (rich in Ca²⁺, oxalate, purines) to reduce urinary deposition.
3. Diet macroCut high-protein & high-fat foods; restrict meat / organ meats to control purine → uric-acid stones.
4. SaltLower salt intake to lessen renal load and solute accumulation.
5. OxalateConsume spinach cautiously (high oxalate → oxalate stones).
SummaryStones 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.

  1. 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.
  2. 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.
  3. 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.

CauseMechanism / Key PointsDiagnostic NoteTreatment & Nursing
Abdominal traumaDirect blow → local oedema / haematoma → peritoneal stripe widensCT to size haematoma / detect tearSmall: conservative; Peritoneal tear: surgical repair
PeritonitisBacterial infection, perforation, intraperitoneal bleed → inflammation & thickening; presents with nausea, vomiting, abdominal painCT ± paracentesis; sepsis work-upIV antibiotics (ceftriaxone, cefoperazone-sulbactam); laparoscopic lavage / repair if needed
Malignant metastasisGastric, colonic, ovarian etc. seeds peritoneum → plaque-like thickeningCT + tumour markers; PET-CT for extentSystemic chemotherapy ± palliative RT; cytoreductive surgery only if good response
General supportive careLight, 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.
SectionKey Messages (English)
Body calcium facts1.5–2 % of body wt (≈ 1 200 g); 99 % in bone/teeth, 1 % in blood; deficiency → growth failure, osteoporosis, pain, weakness.
Lifelong needsChildren, elderly, post-menopausal women & stone-formers must maintain intake.
Old vs new theoryExcess Ca NOT the cause; disordered Ca metabolism mobilises bone Ca → high serum Ca & oxalate still crystallises if urinary oxalate high.
EvidenceLarge UK study: higher Ca intake → lower stone risk; restriction does NOT prevent stones but promotes osteoporosis.
Preferred sourceDiet first: tofu, dairy, small fish with bones, shrimp, marine products (high absorption, low crystallisation risk).
Anti-oxalate tacticsLimit high-oxalate foods; use citrate (citrus drinks/fruit) to compete with oxalate for Ca.
Supplement if neededBio-active Ca (pearl Ca, Caltrate-D, etc.) + vitamin D; avoid poor-absorption salts (gluconate, plain carbonate).
Ca:P ratioMaintain 3:2 with phosphorus-rich foods (milk, eggs, meat, fish, legumes).
Safe dose1–1.5 g/day: improves bone, does NOT worsen stones; > 2 g/day may precipitate in kidney.
Lifestyle during RxAvoid alcohol & coffee; stay well-hydrated.
General preventionDrink 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

  1. 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.
  2. 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.
  3. 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

  1. Functional dyspepsia – dyspeptic symptoms but negative endoscopy/barium study.
  2. Chronic gastritis – irregular upper-abdominal pain; endoscopy shows chronic antral changes.
  3. Zollinger–Ellison (gastrinoma) – BAO > 15 mmol/h, BAO/MAO > 0.6, atypical/multiple refractory ulcers, diarrhoea, serum gastrin > 200 pg/ml (often > 500).
  4. Malignant gastric ulcer/gastric cancer – excluded by endoscopy with biopsy and barium study.
  5. 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.

CategoryKey points (English)
Clinical suspicionRecent persimmon / hawthorn / black-jujube intake + epigastric pain, vomiting, melena.
Laboratory testsMicrocytic anaemia; + faecal occult blood; persimmon-skin debris; ↑ gastric free acid.
X-ray barium studyFree-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.
UltrasonographyAfter 500–1000 mL water: strongly echogenic mass floating in gastric fluid, shifts with posture/peristalsis.
Differential diagnoses1. 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 adviceRegular 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.

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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 intakeDrink plenty of plain water daily to dilute gut/urine content ↓ calcium & oxalate concentration.
2. Functional foodInclude black fungus (wood-ear mushroom) – traditional fiber-rich food believed to soften & dislodge debris.
3. Calcium balanceResume/supplement calcium only as directed by doctor; avoid both deficiency and excess.
4. Vitamin AMaintain adequate intake (broccoli, apricot, cantaloupe, pumpkin, beef liver) to support mucosal health; high-dose supplements toxic—check dose first.
5. General dietLow-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.

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:

  1. 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.
  2. 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.
  3. 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.

AspectKey Points
Intra-operative painAnesthesia provided; pain usually minimal.
Post-operative painUreteral spasm may occur while fragments pass → colicky pain; generally tolerable.
ESWL ≤ 2 cmX-ray/US localization; shock waves pulverize stone to sand, voided with urine.
Ureteroscopy < 2 cmFlexible/rigid scope retrograde; fragment & extract radiolucent or ESWL-resistant stones.
PCNL > 2 cmPercutaneous tract; nephroscopic ultrasonic/laser/pneumatic fragmentation & extraction.
Universal after-careHigh 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.

ItemDetails
Onset of expulsionUsually begins ≥ 1 day after ESWL; soft stones may pass same day.
MechanismFragments are flushed by high fluid intake (2–3 L/day) and physical activity (walking).
Time-courseFirst fragments appear after 24 h; majority clear within 1 day if complete fragmentation achieved.
Hard/large stonesMay require a second session 1 week later; only after further breaking can all fragments pass.
Expected symptomsMild 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.

ItemInstructions / Time-frame
Minimum rest3 days
Why rest?Renal/ureteral edema or small mucosal tears caused by shock waves
Allowed activitiesPlenty of water, gentle walking to help fragments pass
ForbiddenStrenuous exercise (worsens pain & edema)
Review on day 3Imaging check:
• No residual stonesResume normal activity
• Residual stonesSecond ESWL → longer rest
Diet & moodStay relaxed; avoid spicy / irritating foods

How many days of hospitalization are needed after minimally invasive lithotripsy?

In general, minimally invasive lithotripsy requires 5–7 days of hospitalization.

When extracorporeal shock-wave lithotripsy (ESWL) fails to clear the stones, minimally invasive lithotripsy is performed. This involves making a small puncture in the skin to insert a special instrument that delivers holmium laser energy directly onto the stone surface. The success rate is high because the laser effectively fragments most stones, allowing the fragments to pass out naturally.

For ureteral stones, a cystoscope can be passed through the bladder into the ureter to reach the stone, and holmium laser lithotripsy is then performed. Although effective, the procedure may cause minor trauma to surrounding tissues. Therefore, patients are typically hospitalized for 5–7 days post-operatively. During this period:

  • Anti-inflammatory and anti-edema medications are administered.
  • Urine color is monitored; if red blood cells are present, it indicates possible injury to the kidney or ureter, and the patient is advised to drink plenty of water and rest in bed.

If, after 5–7 days, the patient has no discomfort and urine returns to normal, they can be discharged.

Post-discharge instructions:

  • Avoid strenuous exercise
  • Drink large amounts of water to help flush out any remaining fragments.
ItemDetails
ProcedureMinimally invasive lithotripsy (holmium laser) via percutaneous nephrolithotomy or ureteroscopy
IndicationESWL failure or large/impacted stones
Hospital stay5–7 days (standard)
Post-op care in hospital• Anti-inflammatory & anti-edema drugs
• Monitor urine color for RBCs
• Hydration + bed rest if hematuria
Discharge criteriaNo symptoms + clear urine
Home instructionsAvoid strenuous activity; drink plenty of water