- Published on
Surgery - Appendicectomy
An acute case of appendicitis. interval treatment after using IV antibiotics to treat an appendix mass.
Anatomy
2.5 cm below the connection with the terminal ileum, the appendix originates at the convergence of the taeniae coli on the posteromedial side of the caecum. The appendix can lay in the following positions: retrocaecal (70%), pelvic (20%), subcaecal (2%) and pre- or post-ileal (5%). Its length ranges from 1.2 to 22.0 cm. The appendicular artery, a branch of the ileocolic artery, passes via its mesentery, the mesoappendix. To empty into ileocaecal nodes, lymphatics from the appendix pass through the mesoappendix.
Investigations
FBC, U&Es, LFT, amylase, CRP, and urinalysis (to look into stomach pain) are performed prior to surgery. It is recommended that women who are fertile have a pregnancy test done. If sepsis symptoms are present, antibiotics are initiated; if not, a single preventive dosage is administered at the time of operation.
Post-op: If the appendix is inflamed, antibiotics may need to be continued. prophlyaxis for DVT.
Procedure
can be carried out openly or by laparoscopy.
Make sure you always look at the patient on the table to check for any lumps.
Access: The subcutaneous fat is separated and the external oblique aponeurosis is exposed by a Lanz (horizontal skin crease) incision, which is centered on McBurney's point, which is two thirds the distance from the umbilicus to the anterior superior iliac spine.
With scissors, a tiny incision is created in the direction of the fibers. Similar to transversus, internal oblique muscle is divided bluntly along the direction of its fibers, and the opening is gradually widened with retractors.
The peritoneum is carefully lifted up with a clip after it is revealed.
After that, the first clip is moved and a second clip is positioned. Make sure there is no bowel trapped between the clips by palpating the area before making a tiny cut and then extending.
Identification: Pus or free fluid are looked for in the peritoneal cavity. The appendix's base is located by identifying the caecum and following the taeniae, after which it is gently bluntly dissected to release it from inflammatory adhesions. Using Babcock's forceps, the appendix is removed.
Even if the appendix is determined to be normal (or "lily-white"), it should still be removed; still, the small bowel needs to be thoroughly examined to rule out mesenteric adenitis, terminal ileitis, or Meckel's diverticulum.
The right ovary and fallopian tube should be examined in females.
Resection: To maintain hemostasis, the mesoappendix is separated and clipped after being tied off. The appendix's base is crushed with a crushing clamp, and it is then transfixed or tied off before removal. The appendix is transported to be examined histologically. Typically, a purse string suture is used to bury the appendix stump. If there is pus or inflammatory fluid in the cavity, it should be cleaned.
Closure: Subsequently, the incision is layered shut. The peritoneum is sutured continuously, followed by interrupted sutures to the muscle layers and finally continuous sutures to the external oblique—the latter of which is crucial in preventing more hernias. For the skin, a subcuticular absorbable suture is typically utilized. Infiltration of local anesthetic lessens post-operative pain.
Laparoscopic appendicectomy: This alternate method can be both therapeutic and diagnostic, making it particularly helpful for women whose diagnosis may be unclear.
The mesoappendix is separated from the appendix and loop sutured or endostapled across the appendix base before being excised and removed through a port after the capnoperitoneum and port insertion.
Complications
Very rare, but when present indicates the severity of peritonitis or inflammation; examples include ileus, hemorrhage, wound infection, and, less frequently, pelvic or local abscesses.
Prognosis
usually good with mortality less than 1%, however in older adults or in cases of perforation, this may be greater.
An acute case of appendicitis. interval treatment after using IV antibiotics to treat an appendix mass.
Anatomy
2.5 cm below the connection with the terminal ileum, the appendix originates at the convergence of the taeniae coli on the posteromedial side of the caecum. The appendix can lay in the following positions: retrocaecal (70%), pelvic (20%), subcaecal (2%) and pre- or post-ileal (5%). Its length ranges from 1.2 to 22.0 cm. The appendicular artery, a branch of the ileocolic artery, passes via its mesentery, the mesoappendix. To empty into ileocaecal nodes, lymphatics from the appendix pass through the mesoappendix.
Investigations
FBC, U&Es, LFT, amylase, CRP, and urinalysis (to look into stomach pain) are performed prior to surgery. It is recommended that women who are fertile have a pregnancy test done. If sepsis symptoms are present, antibiotics are initiated; if not, a single preventive dosage is administered at the time of operation.
Post-op: If the appendix is inflamed, antibiotics may need to be continued. prophlyaxis for DVT.
Procedure
can be carried out openly or by laparoscopy.
Make sure you always look at the patient on the table to check for any lumps.
Access: The subcutaneous fat is separated and the external oblique aponeurosis is exposed by a Lanz (horizontal skin crease) incision, which is centered on McBurney's point, which is two thirds the distance from the umbilicus to the anterior superior iliac spine.
With scissors, a tiny incision is created in the direction of the fibers. Similar to transversus, internal oblique muscle is divided bluntly along the direction of its fibers, and the opening is gradually widened with retractors.
The peritoneum is carefully lifted up with a clip after it is revealed.
After that, the first clip is moved and a second clip is positioned. Make sure there is no bowel trapped between the clips by palpating the area before making a tiny cut and then extending.
Identification: Pus or free fluid are looked for in the peritoneal cavity. The appendix's base is located by identifying the caecum and following the taeniae, after which it is gently bluntly dissected to release it from inflammatory adhesions. Using Babcock's forceps, the appendix is removed.
Even if the appendix is determined to be normal (or "lily-white"), it should still be removed; still, the small bowel needs to be thoroughly examined to rule out mesenteric adenitis, terminal ileitis, or Meckel's diverticulum.
The right ovary and fallopian tube should be examined in females.
Resection: To maintain hemostasis, the mesoappendix is separated and clipped after being tied off. The appendix's base is crushed with a crushing clamp, and it is then transfixed or tied off before removal. The appendix is transported to be examined histologically. Typically, a purse string suture is used to bury the appendix stump. If there is pus or inflammatory fluid in the cavity, it should be cleaned.
Closure: Subsequently, the incision is layered shut. The peritoneum is sutured continuously, followed by interrupted sutures to the muscle layers and finally continuous sutures to the external oblique—the latter of which is crucial in preventing more hernias. For the skin, a subcuticular absorbable suture is typically utilized. Infiltration of local anesthetic lessens post-operative pain.
Laparoscopic appendicectomy: This alternate method can be both therapeutic and diagnostic, making it particularly helpful for women whose diagnosis may be unclear.
The mesoappendix is separated from the appendix and loop sutured or endostapled across the appendix base before being excised and removed through a port after the capnoperitoneum and port insertion.
Complications
Very rare, but when present indicates the severity of peritonitis or inflammation; examples include ileus, hemorrhage, wound infection, and, less frequently, pelvic or local abscesses.
Prognosis
usually good with mortality less than 1%, however in older adults or in cases of perforation, this may be greater.
- Published on
Surgery - Subdural Hemorrhage
Introduction
A collection of blood that forms between the dura mater and the brain's surface is known as a subdural haematoma (SDH).
Acute: In less than a week.
Subacute: 18 to 24 hours.
Chronic: Three weeks in.
Etiology
Shearing pressures from trauma that causes the brain to accelerate and decelerate quickly rip the "bridging veins," or veins that connect the dura to the cortex. Between the dura and arachnoid membranes, bleeding takes place.
Non-accidental injury in children should always be taken into account.
Epidemiology
Acute: Usually affects younger individuals and is linked to significant trauma (5–25% of cases of severe head injuries). greater in frequency than extradural hemorrhage.
Chronic: Research indicates that the incidence of this condition is 1-2/5/100,000 in the elderly.
History
Acute: Patient has a history of head trauma and is not fully aware.
Subacute: Changing mental status and increasing headaches 7–14 days after injury.
Chronic: May show up as focal weakness, headache, disorientation, cognitive decline, mental symptoms, or seizures.
Have a low index of suspicion, especially in the case of older people and alcoholics, as there may not be a history of trauma or falls.
Examination
Acute: Lower GCS. Large hemorrhages that cause a midline shift can also cause bradycardia, diminished consciousness, and an ipsilateral fixed dilated pupil due to compression of the ipsilateral IIIrd nerve parasympathetic fibres.
Chronic: There may be focal neurological signs (hemiparesis, reflex asymmetry, papilloedema, malfunction of the IIIrd or VIth nerves), but neurological testing may be normal.
Investigations
The CT head is a lump with a crescent or sickle shape that is concave across the surface of the brain (an extradural has a lentiform shape). The CT look varies over time. Chronic subdurals are hypodense (approaching that of CSF) while acute subdurals are hyperdense (becoming isodense over 1-3 weeks; presence may be inferred from indications such as effacement of sulci, midline shift, ventricular compression, and obliteration of basal cisterns).
The brain's MRI is more sensitive, particularly for isodense or tiny SDHs.
Management
Acute: ABC and cervical spine control are given priority in the ATLS procedure. Cervical spine injuries are far more likely to occur following a head injury. GCS and pupillary reactivity are disabilities. Lift your head and think about osmotic diuresis with mannitol and/or hyperventilation if there are indications of an elevated ICP. After stabilization, take the CT head.
Cautious: Particularly when there is a tiny and minor midline shift (SDH <10 mm in thickness and <5 mm in midline shift).
Surgical: For symptomatic subdurals larger than 10 mm, promptly do a burr hole or craniotomy and evacuation, with a midline displacement of more than 5 mm (best if within 4 hours). Devices for ICP monitoring could be installed.
Chronic: Surgical treatment with a burr hole or craniotomy and drainage (a drain may be left in for 24–72 hours) if there is symptomatic or a mass effect on imaging. The recommended course of treatment for asymptomatic SDH without a noticeable mass effect is to use serial imaging to watch for spontaneous resorption. Resorbing hematomas can necessitate a craniotomy along with a membranectomy.
Younger children: If open fontanelle percutaneous aspiration is not successful, a subdural to peritoneal shunt can be implanted.
Complications
Increased intracranial pressure, cerebral edema that may lead to further ischemic brain injury, and mass effect (such as a transtentorial or uncal herniation).
After surgery: The following conditions are relatively common: intracerebral hemorrhage, subdural empyema, meningitis or brain abscess, tension pneumocephalus, seizures, and recurrence (up to 33% for SDH).
Prognosis
Acute: The primary determinant of outcome is the underlying brain damage.
Because there is a lower frequency of underlying brain injury, chronic SDHs often have better results than acute SDHs; three-fourths of patients treated with surgery have satisfactory outcomes.
Introduction
A collection of blood that forms between the dura mater and the brain's surface is known as a subdural haematoma (SDH).
Acute: In less than a week.
Subacute: 18 to 24 hours.
Chronic: Three weeks in.
Etiology
Shearing pressures from trauma that causes the brain to accelerate and decelerate quickly rip the "bridging veins," or veins that connect the dura to the cortex. Between the dura and arachnoid membranes, bleeding takes place.
Non-accidental injury in children should always be taken into account.
Epidemiology
Acute: Usually affects younger individuals and is linked to significant trauma (5–25% of cases of severe head injuries). greater in frequency than extradural hemorrhage.
Chronic: Research indicates that the incidence of this condition is 1-2/5/100,000 in the elderly.
History
Acute: Patient has a history of head trauma and is not fully aware.
Subacute: Changing mental status and increasing headaches 7–14 days after injury.
Chronic: May show up as focal weakness, headache, disorientation, cognitive decline, mental symptoms, or seizures.
Have a low index of suspicion, especially in the case of older people and alcoholics, as there may not be a history of trauma or falls.
Examination
Acute: Lower GCS. Large hemorrhages that cause a midline shift can also cause bradycardia, diminished consciousness, and an ipsilateral fixed dilated pupil due to compression of the ipsilateral IIIrd nerve parasympathetic fibres.
Chronic: There may be focal neurological signs (hemiparesis, reflex asymmetry, papilloedema, malfunction of the IIIrd or VIth nerves), but neurological testing may be normal.
Investigations
The CT head is a lump with a crescent or sickle shape that is concave across the surface of the brain (an extradural has a lentiform shape). The CT look varies over time. Chronic subdurals are hypodense (approaching that of CSF) while acute subdurals are hyperdense (becoming isodense over 1-3 weeks; presence may be inferred from indications such as effacement of sulci, midline shift, ventricular compression, and obliteration of basal cisterns).
The brain's MRI is more sensitive, particularly for isodense or tiny SDHs.
Management
Acute: ABC and cervical spine control are given priority in the ATLS procedure. Cervical spine injuries are far more likely to occur following a head injury. GCS and pupillary reactivity are disabilities. Lift your head and think about osmotic diuresis with mannitol and/or hyperventilation if there are indications of an elevated ICP. After stabilization, take the CT head.
Cautious: Particularly when there is a tiny and minor midline shift (SDH <10 mm in thickness and <5 mm in midline shift).
Surgical: For symptomatic subdurals larger than 10 mm, promptly do a burr hole or craniotomy and evacuation, with a midline displacement of more than 5 mm (best if within 4 hours). Devices for ICP monitoring could be installed.
Chronic: Surgical treatment with a burr hole or craniotomy and drainage (a drain may be left in for 24–72 hours) if there is symptomatic or a mass effect on imaging. The recommended course of treatment for asymptomatic SDH without a noticeable mass effect is to use serial imaging to watch for spontaneous resorption. Resorbing hematomas can necessitate a craniotomy along with a membranectomy.
Younger children: If open fontanelle percutaneous aspiration is not successful, a subdural to peritoneal shunt can be implanted.
Complications
Increased intracranial pressure, cerebral edema that may lead to further ischemic brain injury, and mass effect (such as a transtentorial or uncal herniation).
After surgery: The following conditions are relatively common: intracerebral hemorrhage, subdural empyema, meningitis or brain abscess, tension pneumocephalus, seizures, and recurrence (up to 33% for SDH).
Prognosis
Acute: The primary determinant of outcome is the underlying brain damage.
Because there is a lower frequency of underlying brain injury, chronic SDHs often have better results than acute SDHs; three-fourths of patients treated with surgery have satisfactory outcomes.
- Published on
Surgery - Hemorrhoids
Introduction
Engorged and swollen anal vascular cushions have a propensity to protrude, hemorrhage, or prolapse into the anal canal, which aids in anal closure.
arranged according to location:
.. Internal (originating above the dentate line from the superior hemorrhoidal plexus). External (below dentate line, from inferior hemorrhoidal plexus)
categorized according to prolapse degree:
.. Initial degree: Non-prolapse hemorrhoids. Second degree: Prolapse that occurs with defecation but goes away on its own. Third degree: Prolapse that needs to be manually reduced. Fourth degree: Non-reducible prolapse.
Risk Factors
pregnancy, extended straining, constipation, and portal hypertension.
Epidemiology
Common (4–5% prevalence). The peak age range is 45–65. mostly a Westernized world sickness.
H HISTORY
usually without symptoms.
Bleeding, typically bright red blood, on toilet paper or dripping into a pan following the passage of stool is possible, but it is never mixed in with the stool itself. The absence of warning signs such as weight loss, anemia, altered bowel habits, clotted, black blood, or mucus mixed with feces is necessary. Itching, anal tumors, or prolapsing tissue are other symptoms. When external hemorrhoids thrombose, they can be extremely painful.
Examination
Uncomplicated hemorrhoids are impalpable and only visible on proctoscopy, where they manifest as red, granular mucosal swellings that bulge into view upon straining and withdrawing the proctoscope at 3, 7, and 11 o'clock. First- or second-degree hemorrhoids are typically not visible on external inspection. Anal tags, anal fissure, rectal prolapse, polyps, or tumors are examples of differential diagnosis.
Pathogenesis
Overstretching results in anal engorgement, shearing by hard stools, and downward displacement, which in turn causes hypertrophy and fragmentation of muscle and elastin fibers, disruption of tissue organization, elevated resting anal pressures, and bleeding from pre-sinusoidal arterioles.
Investigations
To rule out a rectal source of bleeding, either a rigid or flexible sigmoidoscopy is typically necessary because hemorrhoids are frequently associated with colorectal tumors.
Management
Conservative: Suggestions for a diet rich in fiber, water consumption, and large laxatives. There are topical lotions that mix a local anesthetic with mild astringents; those that contain corticosteroids should only be applied temporarily.
For first or second degree local therapy: Injection sclerotherapy involves injecting 5% phenol in almond oil into the submucosa above a hemorrhoid, above the dentate line (where sensory fibers are absent), causing inflammation and fibrosis that leads to mucosal fixation. Banding: Barron's bands are placed immediately proximal to the hemorrhage, including tissue that disappears in two to three days, leaving a tiny ulcer to heal naturally. higher chances of recovery but sometimes more agony. Hemorrhoidal artery ligation, radiofrequency ablation, and infrared coagulation are further methods.
Surgical: Saved for third- or fourth-degree hemorrhoids that present with symptoms. In order to prevent stricturing, the Milligan-Morgan open hemorrhoidectomy entails removing the hemorrhoidal cushions while maintaining the skin and mucosal bridges that connect the hemorrhoids. In order to "hitch up" the prolapsing anal lining and interrupt the proximal blood flow, stapled hemorrhoidectomy involves mucosectomy 2 cm proximal to the dentate line (# discomfort and shorter convalescence in randomized control trials). laxatives to prevent constipation after surgery, metronidazole.
Complications
thrombosis, prolapse, and bleeding. Prostatitis, perineal sepsis, hepatic abscesses, retroperitoneal sepsis, and infrequently impotence are side effects of injectable sclerotherapy. Pain, bleeding, recurrence, and, less frequently, incontinence from sphincteric damage and anal stricture following a hemorrhoidectomy.
Prognosis
Frequently a chronic issue requiring repeated local treatments due to symptom recurrence.
Severe symptoms may be permanently relieved by surgery.
Introduction
Engorged and swollen anal vascular cushions have a propensity to protrude, hemorrhage, or prolapse into the anal canal, which aids in anal closure.
arranged according to location:
.. Internal (originating above the dentate line from the superior hemorrhoidal plexus). External (below dentate line, from inferior hemorrhoidal plexus)
categorized according to prolapse degree:
.. Initial degree: Non-prolapse hemorrhoids. Second degree: Prolapse that occurs with defecation but goes away on its own. Third degree: Prolapse that needs to be manually reduced. Fourth degree: Non-reducible prolapse.
Risk Factors
pregnancy, extended straining, constipation, and portal hypertension.
Epidemiology
Common (4–5% prevalence). The peak age range is 45–65. mostly a Westernized world sickness.
H HISTORY
usually without symptoms.
Bleeding, typically bright red blood, on toilet paper or dripping into a pan following the passage of stool is possible, but it is never mixed in with the stool itself. The absence of warning signs such as weight loss, anemia, altered bowel habits, clotted, black blood, or mucus mixed with feces is necessary. Itching, anal tumors, or prolapsing tissue are other symptoms. When external hemorrhoids thrombose, they can be extremely painful.
Examination
Uncomplicated hemorrhoids are impalpable and only visible on proctoscopy, where they manifest as red, granular mucosal swellings that bulge into view upon straining and withdrawing the proctoscope at 3, 7, and 11 o'clock. First- or second-degree hemorrhoids are typically not visible on external inspection. Anal tags, anal fissure, rectal prolapse, polyps, or tumors are examples of differential diagnosis.
Pathogenesis
Overstretching results in anal engorgement, shearing by hard stools, and downward displacement, which in turn causes hypertrophy and fragmentation of muscle and elastin fibers, disruption of tissue organization, elevated resting anal pressures, and bleeding from pre-sinusoidal arterioles.
Investigations
To rule out a rectal source of bleeding, either a rigid or flexible sigmoidoscopy is typically necessary because hemorrhoids are frequently associated with colorectal tumors.
Management
Conservative: Suggestions for a diet rich in fiber, water consumption, and large laxatives. There are topical lotions that mix a local anesthetic with mild astringents; those that contain corticosteroids should only be applied temporarily.
For first or second degree local therapy: Injection sclerotherapy involves injecting 5% phenol in almond oil into the submucosa above a hemorrhoid, above the dentate line (where sensory fibers are absent), causing inflammation and fibrosis that leads to mucosal fixation. Banding: Barron's bands are placed immediately proximal to the hemorrhage, including tissue that disappears in two to three days, leaving a tiny ulcer to heal naturally. higher chances of recovery but sometimes more agony. Hemorrhoidal artery ligation, radiofrequency ablation, and infrared coagulation are further methods.
Surgical: Saved for third- or fourth-degree hemorrhoids that present with symptoms. In order to prevent stricturing, the Milligan-Morgan open hemorrhoidectomy entails removing the hemorrhoidal cushions while maintaining the skin and mucosal bridges that connect the hemorrhoids. In order to "hitch up" the prolapsing anal lining and interrupt the proximal blood flow, stapled hemorrhoidectomy involves mucosectomy 2 cm proximal to the dentate line (# discomfort and shorter convalescence in randomized control trials). laxatives to prevent constipation after surgery, metronidazole.
Complications
thrombosis, prolapse, and bleeding. Prostatitis, perineal sepsis, hepatic abscesses, retroperitoneal sepsis, and infrequently impotence are side effects of injectable sclerotherapy. Pain, bleeding, recurrence, and, less frequently, incontinence from sphincteric damage and anal stricture following a hemorrhoidectomy.
Prognosis
Frequently a chronic issue requiring repeated local treatments due to symptom recurrence.
Severe symptoms may be permanently relieved by surgery.
- Published on
Surgery - Perianal fistula and abscess
Introduction
A collection of pus in the perianal area is called a perianal abscess.
A perianal fistula is an aberrant, persistently infected channel that connects the rectum or anal canal to the skin of the perianal region.
Types of abscesses: Submucous, subcutaneous, intersphincteric, ischiorectal, and pelvirectal abscesses are categorized based on their location.
Types of fistulas: According to Park, there are five different types of sphincters: superficial, transsphincteric, suprasphincteric, extrasphincteric, or low anal (below puborectalis), high anal (at or above puborectalis), and pelvirectal (including levator ani).
Etiology
Superinfection that extends to perianal tissues is caused by obstruction and stasis of the anal crypt glands. Once an abscess discharges or is removed, fistulae may form. They can also result in multiple perineal fistulae (pepperpot perineum), a consequence of Crohn's disease.
perhaps linked to malignancy (rectal cancer) or diabetes.
Epidemiology
peak incidence in the third to fourth decade, common. greater in men.
History
persistent throbbing discomfort in the lower leg. Fistulae cause sporadic discharge that may be blood- or mucus-stained close to the anal area.
Examination
localized, painful swelling of the perianal region or a little skin incision with discharge close to the anus, which is indicative of a fistula opening. One may feel a region of induration on PR that corresponds to the fistula tract or abscess. Not usually feasible because of sphincter spasm or discomfort.
It can be necessary to do an examination while sedated.
The Goodsall Rule: As a general guideline, locate the internal fistula opening based on where the external fistula opening is located. The fistula enters the anal canal directly and radially if the external orifice is ahead of the anal canal. The fistula tract takes a curved route and opens internally at the posterior midline if the external opening is posterior to the anal canal.
Investigations
Blood: if pyrexial, blood cultures, FBC, CRP, and ESR.
When it comes to intricate fistulae, MRI is quite helpful in enabling a thorough examination of the tracts. enables the planning of surgery to guarantee total excision.
Less helpful than MRI, endoanal ultrasound is nevertheless utilized.
Management
Surgical: Necessitates general anesthesia for surgical care.
Open drainage of an abscess: An incision and drainage operation is the most typical method. Over the abscess, a cruciate incision is created. Locus disintegrates and pus is extracted. After that, the cavity is softly packed and irrigated.
Laying open of fistula: The tract is gently explored using a probe. To show the internal opening, inject methylene blue or hydrogen peroxide into the exterior orifice.
Low fistulae: A fistulotomy is used to treat the condition by opening and cutting the tract, curing away granulation tissue, and enabling secondary intention healing.
To prevent the anal sphincter from being harmed, extreme caution must be used.
High fistulae: Surgical solutions are available for fistulae affecting the upper half of the sphincter complex, where muscle division would result in incontinence. A non-absorbable suture called a seton is inserted through the fistula tract to allow sepsis to drain and to progressively cut through the sphincter while maintaining continence. Advancement flap: A mucosal advancement flap closes the internal aperture after the exterior portion of the fistula is removed.
Fistula plug: To promote closure, a xenograft composed of pig intestinal submucosa is placed into the tract. Fibrin glue: Fibrin glue obliterates the fistula tract. Poor long-term outcomes.
Antibiotics: Surgery is the preferred method of treating abscesses; however, if cellulitis is present, antibiotics may be helpful.
Complications
severe sepsis if left untreated, recurrence. incontinence and harm to the anal sphincter following fistula surgery.
Prognosis
high rate of recurrence without total removal. Recurrence rates with advancement flaps for high fistulae range from 0% to 63%.
Introduction
A collection of pus in the perianal area is called a perianal abscess.
A perianal fistula is an aberrant, persistently infected channel that connects the rectum or anal canal to the skin of the perianal region.
Types of abscesses: Submucous, subcutaneous, intersphincteric, ischiorectal, and pelvirectal abscesses are categorized based on their location.
Types of fistulas: According to Park, there are five different types of sphincters: superficial, transsphincteric, suprasphincteric, extrasphincteric, or low anal (below puborectalis), high anal (at or above puborectalis), and pelvirectal (including levator ani).
Etiology
Superinfection that extends to perianal tissues is caused by obstruction and stasis of the anal crypt glands. Once an abscess discharges or is removed, fistulae may form. They can also result in multiple perineal fistulae (pepperpot perineum), a consequence of Crohn's disease.
perhaps linked to malignancy (rectal cancer) or diabetes.
Epidemiology
peak incidence in the third to fourth decade, common. greater in men.
History
persistent throbbing discomfort in the lower leg. Fistulae cause sporadic discharge that may be blood- or mucus-stained close to the anal area.
Examination
localized, painful swelling of the perianal region or a little skin incision with discharge close to the anus, which is indicative of a fistula opening. One may feel a region of induration on PR that corresponds to the fistula tract or abscess. Not usually feasible because of sphincter spasm or discomfort.
It can be necessary to do an examination while sedated.
The Goodsall Rule: As a general guideline, locate the internal fistula opening based on where the external fistula opening is located. The fistula enters the anal canal directly and radially if the external orifice is ahead of the anal canal. The fistula tract takes a curved route and opens internally at the posterior midline if the external opening is posterior to the anal canal.
Investigations
Blood: if pyrexial, blood cultures, FBC, CRP, and ESR.
When it comes to intricate fistulae, MRI is quite helpful in enabling a thorough examination of the tracts. enables the planning of surgery to guarantee total excision.
Less helpful than MRI, endoanal ultrasound is nevertheless utilized.
Management
Surgical: Necessitates general anesthesia for surgical care.
Open drainage of an abscess: An incision and drainage operation is the most typical method. Over the abscess, a cruciate incision is created. Locus disintegrates and pus is extracted. After that, the cavity is softly packed and irrigated.
Laying open of fistula: The tract is gently explored using a probe. To show the internal opening, inject methylene blue or hydrogen peroxide into the exterior orifice.
Low fistulae: A fistulotomy is used to treat the condition by opening and cutting the tract, curing away granulation tissue, and enabling secondary intention healing.
To prevent the anal sphincter from being harmed, extreme caution must be used.
High fistulae: Surgical solutions are available for fistulae affecting the upper half of the sphincter complex, where muscle division would result in incontinence. A non-absorbable suture called a seton is inserted through the fistula tract to allow sepsis to drain and to progressively cut through the sphincter while maintaining continence. Advancement flap: A mucosal advancement flap closes the internal aperture after the exterior portion of the fistula is removed.
Fistula plug: To promote closure, a xenograft composed of pig intestinal submucosa is placed into the tract. Fibrin glue: Fibrin glue obliterates the fistula tract. Poor long-term outcomes.
Antibiotics: Surgery is the preferred method of treating abscesses; however, if cellulitis is present, antibiotics may be helpful.
Complications
severe sepsis if left untreated, recurrence. incontinence and harm to the anal sphincter following fistula surgery.
Prognosis
high rate of recurrence without total removal. Recurrence rates with advancement flaps for high fistulae range from 0% to 63%.
- Published on
Surgery - Rectal Cancer
Introduction
rectal cancer that manifests itself. roughly one-third of colorectal cancers are caused by this.
AET Information Technology
environmental and genetic variables. When genes that inhibit tumor growth become active or oncogenes get activated, the cells are able to evade growth regulatory control.
Neoplasia can develop from severe dysplasia in adenomatous polyps.
Risk Factors
High-fat, low-fiber diet; polyps found in the colon; history of colorectal cancer in the family; inflammatory bowel illness (especially chronic ulcerative colitis). Hereditary non-polyposis colorectal cancer and familial adenomatous polyposis are examples of familial syndromes.
Epidemiology
There are about 14,000 new instances of rectal cancer in the UK every year. 60–65 years old on average at diagnosis. Males are more likely than females to get rectal cancer.
History
Most often, there is rectal bleeding or blood or mucus mixed up with the stools. Rectal masses can also show up as tenesmus, or the sense that the bowel is not completely emptying after a defecate. Through the NHS bowel cancer screening program, patients may come with positive faecal occult blood tests even when they are asymptomatic.
ANALYZATION
Palpable low-lying rectal tumors may be detected during rectal examination, along with indications of anemia, abdominal distension, and obstructive lesions. If hepatomegaly, metastatic illness, or "shifting dullness" of ascites. A rigid sigmoidoscopy ought to be carried out.
Pathogenesis
98% of them are adenocarcinomas. Sarcoma, melanoma, lymphoma, and carcinoid tumors are uncommon additional tumor forms. The TNM staging system or the modified Dukes system are two staging systems.
Investing in education
Blood: tumor markers (CEA), LFT, and FBC (for anemia).
Stool: Checking for occult blood in the feces.
Endoscopy: colonoscopy and sigmoidoscopy. allows for biopsy and visualization. If a little carcinoma is isolated and in situ, polypectomy may also be performed.
Imaging: Endoanal ultrasound, MRI rectum for local staging and treatment planning, CT chest, abdomen, and pelvis staging. PET imaging. Refer to Pathology/Pathogenesis, please.
TNM Staging
TNM Staging
T1 Tumour invades submucosa
T2 Tumour invades muscularis propria
T3 Tumour invades into subserosa, pericolic or perirectal tissue
T4 Tumour invades other organs or through peritoneum
N0 No nodal metastases
N1 Metastases in 1–3 perirectal nodes
N2 Metastases in more than 4 perirectal nodes
N3 Nodal metastases along a vascular trunk
Management
Depending on the stage and coexisting conditions, a multidisciplinary team of radiologists, surgeons, oncologists, gastroenterologists, and pathologists plans the patient's care.
Transanal excision or endoscopic mucosal resection are two treatment options for pedicunculated polyps and tiny, early-stage (in situ or T1) tumors. This should not be utilized if nodal involvement is suspected.
Neoadjuvant radiation and chemotherapy: The high local recurrence rate following surgery can be reduced with preoperative chemotherapy and radiation therapy (long course or short course). Benefits include respectability gain, downstaging, and perhaps sphincter sparing.
Chemotherapy: 5-fluorouracil combination chemotherapy regimens are frequent (e.g. FOLFOX). In cases of metastatic disease, chemotherapy may be combined with bevacizumab (anti-vascular endothelial growth factor, anti-VEGF) and cetuximab (anti-EGFR, anti-epidermal growth factor receptor).
Surgery: Laparoscopic or open methods. Anterior resection (typically a 2 cm defuncting stoma for tumors of the middle and upper rectum, and rarely the lower rectum if clear margins are possible). Total mesorectal excision, or TME, lowers the local recurrence rate in rectal surgery. When the anal sphincter cannot be preserved, abdominal perineal resection is performed.
Pelvic exenteration is a drastic surgery that might be used for advanced tumors or local recurrences. The lower colon and rectum, lower ureters and bladder, internal reproductive organs, perineum, draining lymph nodes, and pelvic peritoneum are all removed in this procedure. Emergency: Proximal stoma may be defunct due to Hartmann's surgery or unresectable tumors.
Complications
Metastatic illness, recurrence, fistula formation, obstruction or perforation of the bowel. side effects related to the course of treatment. Anastomotic leak during surgery. Ileus, bleeding.
Prognosis
After five years, Dukes A and B have survived at 80–90%, 40–70%, 12–40%, and 7–15%, respectively.
With surgically treatable isolated liver metastases, the 5-year survival rate is 25–40%.
Introduction
rectal cancer that manifests itself. roughly one-third of colorectal cancers are caused by this.
AET Information Technology
environmental and genetic variables. When genes that inhibit tumor growth become active or oncogenes get activated, the cells are able to evade growth regulatory control.
Neoplasia can develop from severe dysplasia in adenomatous polyps.
Risk Factors
High-fat, low-fiber diet; polyps found in the colon; history of colorectal cancer in the family; inflammatory bowel illness (especially chronic ulcerative colitis). Hereditary non-polyposis colorectal cancer and familial adenomatous polyposis are examples of familial syndromes.
Epidemiology
There are about 14,000 new instances of rectal cancer in the UK every year. 60–65 years old on average at diagnosis. Males are more likely than females to get rectal cancer.
History
Most often, there is rectal bleeding or blood or mucus mixed up with the stools. Rectal masses can also show up as tenesmus, or the sense that the bowel is not completely emptying after a defecate. Through the NHS bowel cancer screening program, patients may come with positive faecal occult blood tests even when they are asymptomatic.
ANALYZATION
Palpable low-lying rectal tumors may be detected during rectal examination, along with indications of anemia, abdominal distension, and obstructive lesions. If hepatomegaly, metastatic illness, or "shifting dullness" of ascites. A rigid sigmoidoscopy ought to be carried out.
Pathogenesis
98% of them are adenocarcinomas. Sarcoma, melanoma, lymphoma, and carcinoid tumors are uncommon additional tumor forms. The TNM staging system or the modified Dukes system are two staging systems.
Investing in education
Blood: tumor markers (CEA), LFT, and FBC (for anemia).
Stool: Checking for occult blood in the feces.
Endoscopy: colonoscopy and sigmoidoscopy. allows for biopsy and visualization. If a little carcinoma is isolated and in situ, polypectomy may also be performed.
Imaging: Endoanal ultrasound, MRI rectum for local staging and treatment planning, CT chest, abdomen, and pelvis staging. PET imaging. Refer to Pathology/Pathogenesis, please.
TNM Staging
TNM Staging
T1 Tumour invades submucosa
T2 Tumour invades muscularis propria
T3 Tumour invades into subserosa, pericolic or perirectal tissue
T4 Tumour invades other organs or through peritoneum
N0 No nodal metastases
N1 Metastases in 1–3 perirectal nodes
N2 Metastases in more than 4 perirectal nodes
N3 Nodal metastases along a vascular trunk
Management
Depending on the stage and coexisting conditions, a multidisciplinary team of radiologists, surgeons, oncologists, gastroenterologists, and pathologists plans the patient's care.
Transanal excision or endoscopic mucosal resection are two treatment options for pedicunculated polyps and tiny, early-stage (in situ or T1) tumors. This should not be utilized if nodal involvement is suspected.
Neoadjuvant radiation and chemotherapy: The high local recurrence rate following surgery can be reduced with preoperative chemotherapy and radiation therapy (long course or short course). Benefits include respectability gain, downstaging, and perhaps sphincter sparing.
Chemotherapy: 5-fluorouracil combination chemotherapy regimens are frequent (e.g. FOLFOX). In cases of metastatic disease, chemotherapy may be combined with bevacizumab (anti-vascular endothelial growth factor, anti-VEGF) and cetuximab (anti-EGFR, anti-epidermal growth factor receptor).
Surgery: Laparoscopic or open methods. Anterior resection (typically a 2 cm defuncting stoma for tumors of the middle and upper rectum, and rarely the lower rectum if clear margins are possible). Total mesorectal excision, or TME, lowers the local recurrence rate in rectal surgery. When the anal sphincter cannot be preserved, abdominal perineal resection is performed.
Pelvic exenteration is a drastic surgery that might be used for advanced tumors or local recurrences. The lower colon and rectum, lower ureters and bladder, internal reproductive organs, perineum, draining lymph nodes, and pelvic peritoneum are all removed in this procedure. Emergency: Proximal stoma may be defunct due to Hartmann's surgery or unresectable tumors.
Complications
Metastatic illness, recurrence, fistula formation, obstruction or perforation of the bowel. side effects related to the course of treatment. Anastomotic leak during surgery. Ileus, bleeding.
Prognosis
After five years, Dukes A and B have survived at 80–90%, 40–70%, 12–40%, and 7–15%, respectively.
With surgically treatable isolated liver metastases, the 5-year survival rate is 25–40%.
- Published on
Surgery - Rectal Prolapse
Introduction
the whole thickness rectal wall or aberrant rectal mucosa protrusion through the anus.
Etiology
Incomplete prolapse: This condition, which affects only the mucosa and can occur in both adults and children, is linked to hemorrhoids, constipation, and prolonged straining.
Total prolapse: primarily affects adults and involves the entire rectal wall. It is linked to weak pelvic and anal muscles. Constipation, aging, persistent straining, paralysis of the sphincter, neurological disorders such multiple sclerosis, and childhood cystic fibrosis.
Epidemiology
comparatively typical. There are two peaks: in younger children (male: female) and in older people (female: male is 6: 1).
History
Bulging anal mass that could need to be replaced digitally. hemorrhage from PR related to constipation, faecal incontinence, or mucus passage. may show up as an emergency if the prolapse is strangulated or intractable.
Examination
Straining may reveal the prolapse, which ranges in intensity from protruding rectal mucosa to a full-blown rectal prolapse (if >5 cm, always a complete prolapse). may exhibit necrosis or develop ulcers if the vascular supply is impaired.
lower tone of the anal sphincter.
Investigations
Imaging methods include barium enema, defaecating proctogram, and protosigmoidoscopy.
Further: Pudendal nerve research, anal sphincter manometry.
Sweat chloride test: Approximately 10% of children will test positive for cystic fibrosis.
Management
Conservative: Using a lot of laxatives to treat constipation. A high-fiber diet combined with constipation medication is typically adequate for children.
Emergency: If sufficient analgesia is provided, acute prolapse can be manually controlled. Patients will likely have considerable edema and should be treated with ice packs topically before attempting manual reduction. If the bowel is gangrenous, a rectosigmoidectomy will be necessary.
Surgical: Incomplete prolapse: Mucosal banding, hemorrhoidectomy, or submucosal injection sclerotherapy using phenol in oil are possible options.
Total prolapse: Laparoscopic, abdominal, or perineal methods of surgical repair; for example, Ripstein rectopexy, in which the rectum is mobilized and fixed to the sacrum using nonabsorbable sutures. Resection rectopexy, also known as Delorme's operation, involves plication of the rectal muscle beneath the excised rectal mucosa. In certain situations, anal sphincter repair may be necessary. The Altemeir surgery involves coloanal anastomosis and the resection of the prolapsed rectum and sigmoid colon from below.
Complications
incontinence, rectal bleeding, and mucosal ulcers. Rarely, prolapsed colon necrosis and strangulation.
Prognosis
Children typically experience spontaneous resolution. Generally favorable in adults with appropriate treatment, although there is a 15% recurrence rate.
Introduction
the whole thickness rectal wall or aberrant rectal mucosa protrusion through the anus.
Etiology
Incomplete prolapse: This condition, which affects only the mucosa and can occur in both adults and children, is linked to hemorrhoids, constipation, and prolonged straining.
Total prolapse: primarily affects adults and involves the entire rectal wall. It is linked to weak pelvic and anal muscles. Constipation, aging, persistent straining, paralysis of the sphincter, neurological disorders such multiple sclerosis, and childhood cystic fibrosis.
Epidemiology
comparatively typical. There are two peaks: in younger children (male: female) and in older people (female: male is 6: 1).
History
Bulging anal mass that could need to be replaced digitally. hemorrhage from PR related to constipation, faecal incontinence, or mucus passage. may show up as an emergency if the prolapse is strangulated or intractable.
Examination
Straining may reveal the prolapse, which ranges in intensity from protruding rectal mucosa to a full-blown rectal prolapse (if >5 cm, always a complete prolapse). may exhibit necrosis or develop ulcers if the vascular supply is impaired.
lower tone of the anal sphincter.
Investigations
Imaging methods include barium enema, defaecating proctogram, and protosigmoidoscopy.
Further: Pudendal nerve research, anal sphincter manometry.
Sweat chloride test: Approximately 10% of children will test positive for cystic fibrosis.
Management
Conservative: Using a lot of laxatives to treat constipation. A high-fiber diet combined with constipation medication is typically adequate for children.
Emergency: If sufficient analgesia is provided, acute prolapse can be manually controlled. Patients will likely have considerable edema and should be treated with ice packs topically before attempting manual reduction. If the bowel is gangrenous, a rectosigmoidectomy will be necessary.
Surgical: Incomplete prolapse: Mucosal banding, hemorrhoidectomy, or submucosal injection sclerotherapy using phenol in oil are possible options.
Total prolapse: Laparoscopic, abdominal, or perineal methods of surgical repair; for example, Ripstein rectopexy, in which the rectum is mobilized and fixed to the sacrum using nonabsorbable sutures. Resection rectopexy, also known as Delorme's operation, involves plication of the rectal muscle beneath the excised rectal mucosa. In certain situations, anal sphincter repair may be necessary. The Altemeir surgery involves coloanal anastomosis and the resection of the prolapsed rectum and sigmoid colon from below.
Complications
incontinence, rectal bleeding, and mucosal ulcers. Rarely, prolapsed colon necrosis and strangulation.
Prognosis
Children typically experience spontaneous resolution. Generally favorable in adults with appropriate treatment, although there is a 15% recurrence rate.
- Published on
Surgery - Toxic Megacolon
Introduction
severe colitis accompanied by partial or complete colon dilatation.
Etiology
Most frequently brought on by a severe flare-up of ulcerative colitis, but it can also happen in cases of Crohn's disease, pseudo-membranous colitis (an infection caused by Clostridium difficile), and other infectious colitis.
Epidemiology
May appear in 3–10% of ulcerative colitis patients, less frequently in Crohn's disease patients, and rarely in infections aetiologies.
H HISTORY
The patient has discomfort and cramping in her abdomen and is generally ill. a sudden and violent diarrhea.
Examination
hypotension, tachycardia, dehydration, and pyrexia. a sensitive, swollen abdomen, or a decrease in bowel movements.
Pathogenesis
The gut wall's muscular layers are affected by inflammation. The colon becomes distended and there is a danger of perforation due to neurogenic loss of motor tone. On histological examination, mucosal sloughing, tissue necrosis, and muscle weakening are observed. Systemic poisoning results from colonic bacterial overgrowth absorbed through inflamed colonic mucosa.
Investigations
Blood: significantly elevated WCC, lowered K+ in U&Es, lowered Alb, and elevated CRP.
Radiology: A dilated colon (>6 cm) will be visible on an AXR or CT scan. There is a considerable probability of perforation if the measurement is greater than 10 cm. An erect CXR should be done to look for air under the diaphragm, which would indicate a perforation. It is not recommended to use barium enema since it could puncture.
Managaement
Medical: Multidisciplinary care with the assistance of surgeons, gastroenterologists, and critical care is the best way to manage severe colitis. Depending on the cause, aggressive fluid resuscitation and intravenous antibiotics with or without steroids are recommended. It is possible to utilize IV cyclosporine therapy for ulcerative colitis. In spite of medicinal therapy reasons for surgery, early and routine surgical assessment is crucial when there is clinical deterioration and increasing dilatation on serial abdominal radiographs.
Surgical: Thirty percent of patients seek for urgent care. In most situations, an ileostomy combined with a total colectomy is the best course of surgery.
Complications
rupture as well as peritonitis. Sepsis systemic.
Prognosis
high death rate (20–30%), particularly in cases of perforation
Introduction
severe colitis accompanied by partial or complete colon dilatation.
Etiology
Most frequently brought on by a severe flare-up of ulcerative colitis, but it can also happen in cases of Crohn's disease, pseudo-membranous colitis (an infection caused by Clostridium difficile), and other infectious colitis.
Epidemiology
May appear in 3–10% of ulcerative colitis patients, less frequently in Crohn's disease patients, and rarely in infections aetiologies.
H HISTORY
The patient has discomfort and cramping in her abdomen and is generally ill. a sudden and violent diarrhea.
Examination
hypotension, tachycardia, dehydration, and pyrexia. a sensitive, swollen abdomen, or a decrease in bowel movements.
Pathogenesis
The gut wall's muscular layers are affected by inflammation. The colon becomes distended and there is a danger of perforation due to neurogenic loss of motor tone. On histological examination, mucosal sloughing, tissue necrosis, and muscle weakening are observed. Systemic poisoning results from colonic bacterial overgrowth absorbed through inflamed colonic mucosa.
Investigations
Blood: significantly elevated WCC, lowered K+ in U&Es, lowered Alb, and elevated CRP.
Radiology: A dilated colon (>6 cm) will be visible on an AXR or CT scan. There is a considerable probability of perforation if the measurement is greater than 10 cm. An erect CXR should be done to look for air under the diaphragm, which would indicate a perforation. It is not recommended to use barium enema since it could puncture.
Managaement
Medical: Multidisciplinary care with the assistance of surgeons, gastroenterologists, and critical care is the best way to manage severe colitis. Depending on the cause, aggressive fluid resuscitation and intravenous antibiotics with or without steroids are recommended. It is possible to utilize IV cyclosporine therapy for ulcerative colitis. In spite of medicinal therapy reasons for surgery, early and routine surgical assessment is crucial when there is clinical deterioration and increasing dilatation on serial abdominal radiographs.
Surgical: Thirty percent of patients seek for urgent care. In most situations, an ileostomy combined with a total colectomy is the best course of surgery.
Complications
rupture as well as peritonitis. Sepsis systemic.
Prognosis
high death rate (20–30%), particularly in cases of perforation
- Published on
Surgery - Ulcerative Colitis
Overview
big bowel-related inflammatory illness that is chronic, recurrent, and intermittent.
Etiology
Not sure. The immune system's reaction to bacterial or self-antigens, environmental variables, altered neutrophil function, and abnormalities in epithelial cell integrity are among the theories. Genetic vulnerability (chromosomes 12, 16) is another.
15% had a positive family history of IBD. correlated with primary sclerosing cholangitis and elevated serum pANCA.
Epidemiology
1/1500 is the prevalence (in the developed world). greater frequency in Caucasians and Ashkenazi Jews.
Rare prior to age 10, peak onset age between 20 and 40 years. equal gender ratio until age 40, after which it rises for men.
History
mucous or bloody diarrhea (frequency of stools correlated with disease severity). Urgency and tenesmus. Abdominal cramps before to bowel movement, fever, and weight loss. Extra-GI manifestations' symptoms.
Examination
Indices of low iron levels dehydration and anemia. Clubbing. discomfort in the abdomen and tachycardia.
On a PR examination, there is blood, mucus, and soreness. symptoms that are extra-gastrointestinal.
Investigations
Blood: reduced albumin, elevated CRP or ESR, increased WCC, decreased Hb, crossmatch if significant blood loss, and LFT.
Stool: A differential diagnosis of infectious colitis is culture. The illness severity marker faecal calprotectin.
AXR: To exclude megacolon that is hazardous (see hazardous Megacolon).
Colonoscopy or flexible sigmoidoscopy (including biopsy): assesses dysplasia identification, severity, and histological confirmation.
Barium enema: lack of haustral pattern (lead-pipe or hosepipe look), featureless constricted colon, mucosal ulcers with granular appearance and filling deficiencies (pseudopolyps) (see Fig. 13). In cases of acute exacerbations, colonoscopy and barium enema may be hazardous (risk of perforation).
Management
Activity markers include decreased Hb and Alb, elevated ESR or CRP, and frequency of diarrhea (less than four is mild, four to six is moderate, and more than six is severe), bleeding, and fever.
Acute exacerbation: parenteral nutrition may be required, antibiotics, IV rehydration, IV corticosteroids, bowel rest, and DVT prevention. Keep a careful eye on your vital signs and fluid balance. Low threshold for proctocolectomy and ileostomy if toxic megacolon develops, as perforation has a thirty percent death rate.
Reversible illness: rectal steroids and/or oral 5-aminosalicylic acid (5-ASA) derivatives, such as sulphasalazine. Oral 5-ASA and oral prednisone for moderate-to-severe illness. Azathioprine, cyclosporine, 6-mercaptopurine, and infliximab (anti-TNF monoclonal antibody) induce immunosuppression.
Suggestion: Educating and supporting patients. management of the consequences. routine colonoscopy observation.
Surgical: Recommended in cases where medical treatment fails, problems arise, or colonic cancer is to be prevented. Ileostomy with proctocolectomy or development of an ileoanal pouch
Complications
Digestive: bleeding, poisonous megacolon, splinter, colonic cancer (in patients with advanced disease for more than a decade), gallstones, and PSC.
The following extra-gastrointestinal symptoms (10–20%) include amyloidosis, arthropathy, renal calculi, sacroiliitis, erythema nodosum, pyoderma gangrenosum, osteoporosis (due to steroid treatment), and ankylosing spondylitis.
Prognosis
a normal life expectancy condition that relapses and resolves periodically.
The following are poor prognostic variables (ABCDEF): fever (>38 °C in the first 24 hours), dilated bowel loops, elevated CRP, blood pressure, elevated albumin (<30 g/L), and intestinal dilation.
Overview
big bowel-related inflammatory illness that is chronic, recurrent, and intermittent.
Etiology
Not sure. The immune system's reaction to bacterial or self-antigens, environmental variables, altered neutrophil function, and abnormalities in epithelial cell integrity are among the theories. Genetic vulnerability (chromosomes 12, 16) is another.
15% had a positive family history of IBD. correlated with primary sclerosing cholangitis and elevated serum pANCA.
Epidemiology
1/1500 is the prevalence (in the developed world). greater frequency in Caucasians and Ashkenazi Jews.
Rare prior to age 10, peak onset age between 20 and 40 years. equal gender ratio until age 40, after which it rises for men.
History
mucous or bloody diarrhea (frequency of stools correlated with disease severity). Urgency and tenesmus. Abdominal cramps before to bowel movement, fever, and weight loss. Extra-GI manifestations' symptoms.
Examination
Indices of low iron levels dehydration and anemia. Clubbing. discomfort in the abdomen and tachycardia.
On a PR examination, there is blood, mucus, and soreness. symptoms that are extra-gastrointestinal.
Investigations
Blood: reduced albumin, elevated CRP or ESR, increased WCC, decreased Hb, crossmatch if significant blood loss, and LFT.
Stool: A differential diagnosis of infectious colitis is culture. The illness severity marker faecal calprotectin.
AXR: To exclude megacolon that is hazardous (see hazardous Megacolon).
Colonoscopy or flexible sigmoidoscopy (including biopsy): assesses dysplasia identification, severity, and histological confirmation.
Barium enema: lack of haustral pattern (lead-pipe or hosepipe look), featureless constricted colon, mucosal ulcers with granular appearance and filling deficiencies (pseudopolyps) (see Fig. 13). In cases of acute exacerbations, colonoscopy and barium enema may be hazardous (risk of perforation).
Management
Activity markers include decreased Hb and Alb, elevated ESR or CRP, and frequency of diarrhea (less than four is mild, four to six is moderate, and more than six is severe), bleeding, and fever.
Acute exacerbation: parenteral nutrition may be required, antibiotics, IV rehydration, IV corticosteroids, bowel rest, and DVT prevention. Keep a careful eye on your vital signs and fluid balance. Low threshold for proctocolectomy and ileostomy if toxic megacolon develops, as perforation has a thirty percent death rate.
Reversible illness: rectal steroids and/or oral 5-aminosalicylic acid (5-ASA) derivatives, such as sulphasalazine. Oral 5-ASA and oral prednisone for moderate-to-severe illness. Azathioprine, cyclosporine, 6-mercaptopurine, and infliximab (anti-TNF monoclonal antibody) induce immunosuppression.
Suggestion: Educating and supporting patients. management of the consequences. routine colonoscopy observation.
Surgical: Recommended in cases where medical treatment fails, problems arise, or colonic cancer is to be prevented. Ileostomy with proctocolectomy or development of an ileoanal pouch
Complications
Digestive: bleeding, poisonous megacolon, splinter, colonic cancer (in patients with advanced disease for more than a decade), gallstones, and PSC.
The following extra-gastrointestinal symptoms (10–20%) include amyloidosis, arthropathy, renal calculi, sacroiliitis, erythema nodosum, pyoderma gangrenosum, osteoporosis (due to steroid treatment), and ankylosing spondylitis.
Prognosis
a normal life expectancy condition that relapses and resolves periodically.
The following are poor prognostic variables (ABCDEF): fever (>38 °C in the first 24 hours), dilated bowel loops, elevated CRP, blood pressure, elevated albumin (<30 g/L), and intestinal dilation.
- Published on
Surgery - Colonic Volvulus
Introduction
intestinal blockage and possible ischaemia caused by the bowel's loop rotating around its mesentery axis. Adults typically experience symptoms in the sigmoid colon (65%) and caecum (30%).
Etiology
Anatomical factors include lengthy sigmoid mesentery, movable caecum, debility and chronic constipation, aging, high residue diet, tumor, adhesions, and colonic Chagas disease.
Epidemiology
Causes 5–10% of large bowel obstructions, which are more prevalent in older adults.
History
Vomiting after experiencing severe constipation, abdominal pain, and edema. There can be a history of earlier incidents that ended on their own.
Examination
Symptoms of intestinal obstruction, including pain and distension in the abdomen. Bowel noises are absent or tinkling.
Pathogenesis
A partial or total closed loop obstruction is caused by the bowel segment rotating. The bowel's veins are crushed and obstructed by a 360-degree twist, which can cause circulation problems, gangrene, and perforation if left untreated.
Investigations
AXR: Widely expanded colon loop, maybe resembling a coffee bean. The coffee bean's concavity points to the left in sigmoid volvulus and to the right lower quadrant in caecal volvulus.
may be linked to distal collapse and proximally dilated colon loops.
Contrast enema soluble in water: indicates the location of the obstruction; in sigmoid volvulus, the distal bowel narrows spirally at the region of the deformity, resembling a bird's beak or ace of spades.
CT scan: Shows indications of intestinal ischaemia and rotation of the mesentery and colon.
Management
Resuscitations: IV fluids, NGtube if vomiting, nil by mouth, and IV antibiotics if there are signs of sepsis or ischaemia.
Endoscopic: Flexible sigmoidoscopic decompression or sigmoidoscopy combined with rectal tube insertion can be used to treat sigmoid volvulus. Patients with troublesome recurrent sigmoid volvulus who are unsuitable for surgery may undergo sigmoid fixation with endoscopic insertion of a percutaneous sigmoidostomy tube.
Surgical: Laparotomy, untwisting, excision of dilated, gangrenous, or ischemic colon, with either a primary anastomosis and/or stoma creation, if symptoms of peritonitis, bowel ischaemia, or failure of conservative therapies are present. Right hemicolectomy, caecopexy, ileocaecal resection, or caecal volvulus are the procedures used. An open or laparoscopic sigmoid colectomy can be used to treat recurrent sigmoid volvulus.
Complications
Bowel perforation, toxaemia, gangrene and ischaemia, and peritonitis.
Prognosis
Although sigmoid volvulus can be effectively managed conservatively or endoscopically, recurrence is frequently observed. The overall death rate may reach 20%.
Introduction
intestinal blockage and possible ischaemia caused by the bowel's loop rotating around its mesentery axis. Adults typically experience symptoms in the sigmoid colon (65%) and caecum (30%).
Etiology
Anatomical factors include lengthy sigmoid mesentery, movable caecum, debility and chronic constipation, aging, high residue diet, tumor, adhesions, and colonic Chagas disease.
Epidemiology
Causes 5–10% of large bowel obstructions, which are more prevalent in older adults.
History
Vomiting after experiencing severe constipation, abdominal pain, and edema. There can be a history of earlier incidents that ended on their own.
Examination
Symptoms of intestinal obstruction, including pain and distension in the abdomen. Bowel noises are absent or tinkling.
Pathogenesis
A partial or total closed loop obstruction is caused by the bowel segment rotating. The bowel's veins are crushed and obstructed by a 360-degree twist, which can cause circulation problems, gangrene, and perforation if left untreated.
Investigations
AXR: Widely expanded colon loop, maybe resembling a coffee bean. The coffee bean's concavity points to the left in sigmoid volvulus and to the right lower quadrant in caecal volvulus.
may be linked to distal collapse and proximally dilated colon loops.
Contrast enema soluble in water: indicates the location of the obstruction; in sigmoid volvulus, the distal bowel narrows spirally at the region of the deformity, resembling a bird's beak or ace of spades.
CT scan: Shows indications of intestinal ischaemia and rotation of the mesentery and colon.
Management
Resuscitations: IV fluids, NGtube if vomiting, nil by mouth, and IV antibiotics if there are signs of sepsis or ischaemia.
Endoscopic: Flexible sigmoidoscopic decompression or sigmoidoscopy combined with rectal tube insertion can be used to treat sigmoid volvulus. Patients with troublesome recurrent sigmoid volvulus who are unsuitable for surgery may undergo sigmoid fixation with endoscopic insertion of a percutaneous sigmoidostomy tube.
Surgical: Laparotomy, untwisting, excision of dilated, gangrenous, or ischemic colon, with either a primary anastomosis and/or stoma creation, if symptoms of peritonitis, bowel ischaemia, or failure of conservative therapies are present. Right hemicolectomy, caecopexy, ileocaecal resection, or caecal volvulus are the procedures used. An open or laparoscopic sigmoid colectomy can be used to treat recurrent sigmoid volvulus.
Complications
Bowel perforation, toxaemia, gangrene and ischaemia, and peritonitis.
Prognosis
Although sigmoid volvulus can be effectively managed conservatively or endoscopically, recurrence is frequently observed. The overall death rate may reach 20%.
- Published on
Surgery - Cord Compression and Injury
Introduction
damage to the spinal cord, the location and severity of which will determine the neurological symptoms. Acute compression of the cord is urgent.
Etiology
Direct trauma-related contusion to the spinal cord;-compression due to bone/disc fragmentation or trauma-related hemorrhage;-compression due to extrinsic lesions, such as: disc protrusion; tumors (primary, secondary, or myeloma); spinal abscesses (such as TB and staphylococcus) abnormalities of the spinal vessels
Epidemiology
Typical. All age groups experience trauma. In senior age groups, cancer and disc disease are more prevalent.
History
Past medical history of trauma, illness, or damage.
weakness, pain, and loss of senses.
interruption of bladder or bowel function. impotence.
Urinary retention, saddle anesthesia, and bilateral sciatica are symptoms of cauda-equina syndrome.
Seen in spinal cord hemisection: Brown-Sequard syndrome. ipsilateral leg weakness and contralateral leg numbness.
Examination
Take a close look at both the motor and sensory levels.
Trauma to the spinal cord: Early hyperacute symptoms include diaphragmatic breathing, diminished anal tone, hyporeflexia, priapism, and spinal shock (# BP without tachycardia).
Flaccid paraparesis, urine retention, decreased anal tone, saddle anesthesia, and compromised knee, ankle, and bulbocavernous reflexes are all symptoms of cauda-equina syndrome. Perhaps not symmetrical.
Urinary retention combined with flaccid and spastic paraparesis is known as Conus medullaris syndrome.
Below the lesion, hypertonicity and hyperreflexia are present. Sensory disruption is often symmetrical and distributed perianally.
Sequard-Brown syndrome: observed in spinal cord hemisection. Ipsilateral spastic paralysis, loss of postural sensation, and contralateral loss of pain and temperature sense occur below the level of the lesion.
Differentiate between radiculopathies and cord compression: Radiculopathies are brought on by compression of the nerve root at the exit foramina or in the spinal canal. Only at that motor and sensory level does this result in LMN damage; beyond that level, no UMN indications are present.
Motor
C3–C5: Diaphragm L2: Hip flexion
C5: Shoulder abduction. L3: Knee extension
C6: Forearm flexion L4: Ankle dorsiflexion
C7: Forearm extension L5: Big toe extension
C8: Wrist/finger flexion S1: Ankle plantar flexion
T1: Finger abduction
Reflexes
C5–C6: Biceps reflex L1–L2: Cremaster reflex
C6: Brachioradialis (supinator) reflex L3–L4: Knee reflex
C7: Triceps reflex S1–S2: Ankle reflex
Hoffmann/s sign: UMN in upper limb S2–S4: Anocutaneous refl
S2–S4: Bulbocavernous reflex
Sensory
C4: Supraclavicular fossa T10: Umbilicus
C5: Clavicles T12: Hip girdle
C6: Thumb L4: Medial malleolus
C7: Middle finger S1: Lateral malleolus
C8: Little finger S2: Scrotum
T4: Nipples S3–S5: Perianal region
Investigations
Trauma radiology includes AP and lateral spine (also known as peg view), thoracic, and lumbar radiographs. High-resolution CT scans of the spine, which enable formatting for 3D visualization, are gradually replacing them.
Spine emergency MRI: To see the cord and soft tissue. Changes in cord signal and canal stenosis are important indicators.
Blood: protein electrophoresis, Ca2+, ESR, bone profile, FBC, and U&E.
Bence Jones protein in the urine is a sign of multiple myeloma.
Management
Traumatic cord injury: The ATLS recommendations should be followed while managing trauma injuries.
While it is debatable, NASCIS trial data suggests that giving high-dose steroids (methylprednisolone) to patients with severe spinal cord injuries for less than eight hours can improve their motor function.
Cord compression: If a tumor is found after imaging, high-dose steroids, such as dexamethasone, should be administered as away to lessen cord compression. Emergency radiation may potentially be effective in treating tumors. Get guidance from a neurosurgeon.
Surgery: Often required to remove the origin of compression and/or relieve compression.
External surgical stabilization: Using a halo or traction device, for instance.
Internal surgical stabilization: Using metal implants or bone grafts, for instance.
Surgical decompression: To relieve compression, a laminectomy, for instance.
For disc prolapses, a discectomy or microdiscectomy is used.
Rehabilitation: A multidisciplinary rehabilitation program including occupational therapy and physiotherapy, ideally in a specialized spinal unit.
Complications
Spinal function below the lesion is lost in cases of severe injury.
Paralysis of the breathing system: lesion above C4.
Quadriplegia, C4–T1.
Mid-thoracic: If above T6, paraplegia and autonomic dysreflexia.
S1: Loss of rectum and bladder control due to sacral parasympathetic loss.
Immobility-related complications include pressure sores, DVT, long-term spasticity (posing a risk of deformity), and heterotopic ossification.
Prognosis
When converted to the Frankel grade, the American Spinal Injury Association (ASIA) Impairment Scale after 72 hours after the injury has prognostic significance (see www.asia-spinalinjury.org for score sheet). Depending on the extent of the spinal cord injury, there may be some improvement over time.
Introduction
damage to the spinal cord, the location and severity of which will determine the neurological symptoms. Acute compression of the cord is urgent.
Etiology
Direct trauma-related contusion to the spinal cord;-compression due to bone/disc fragmentation or trauma-related hemorrhage;-compression due to extrinsic lesions, such as: disc protrusion; tumors (primary, secondary, or myeloma); spinal abscesses (such as TB and staphylococcus) abnormalities of the spinal vessels
Epidemiology
Typical. All age groups experience trauma. In senior age groups, cancer and disc disease are more prevalent.
History
Past medical history of trauma, illness, or damage.
weakness, pain, and loss of senses.
interruption of bladder or bowel function. impotence.
Urinary retention, saddle anesthesia, and bilateral sciatica are symptoms of cauda-equina syndrome.
Seen in spinal cord hemisection: Brown-Sequard syndrome. ipsilateral leg weakness and contralateral leg numbness.
Examination
Take a close look at both the motor and sensory levels.
Trauma to the spinal cord: Early hyperacute symptoms include diaphragmatic breathing, diminished anal tone, hyporeflexia, priapism, and spinal shock (# BP without tachycardia).
Flaccid paraparesis, urine retention, decreased anal tone, saddle anesthesia, and compromised knee, ankle, and bulbocavernous reflexes are all symptoms of cauda-equina syndrome. Perhaps not symmetrical.
Urinary retention combined with flaccid and spastic paraparesis is known as Conus medullaris syndrome.
Below the lesion, hypertonicity and hyperreflexia are present. Sensory disruption is often symmetrical and distributed perianally.
Sequard-Brown syndrome: observed in spinal cord hemisection. Ipsilateral spastic paralysis, loss of postural sensation, and contralateral loss of pain and temperature sense occur below the level of the lesion.
Differentiate between radiculopathies and cord compression: Radiculopathies are brought on by compression of the nerve root at the exit foramina or in the spinal canal. Only at that motor and sensory level does this result in LMN damage; beyond that level, no UMN indications are present.
Motor
C3–C5: Diaphragm L2: Hip flexion
C5: Shoulder abduction. L3: Knee extension
C6: Forearm flexion L4: Ankle dorsiflexion
C7: Forearm extension L5: Big toe extension
C8: Wrist/finger flexion S1: Ankle plantar flexion
T1: Finger abduction
Reflexes
C5–C6: Biceps reflex L1–L2: Cremaster reflex
C6: Brachioradialis (supinator) reflex L3–L4: Knee reflex
C7: Triceps reflex S1–S2: Ankle reflex
Hoffmann/s sign: UMN in upper limb S2–S4: Anocutaneous refl
S2–S4: Bulbocavernous reflex
Sensory
C4: Supraclavicular fossa T10: Umbilicus
C5: Clavicles T12: Hip girdle
C6: Thumb L4: Medial malleolus
C7: Middle finger S1: Lateral malleolus
C8: Little finger S2: Scrotum
T4: Nipples S3–S5: Perianal region
Investigations
Trauma radiology includes AP and lateral spine (also known as peg view), thoracic, and lumbar radiographs. High-resolution CT scans of the spine, which enable formatting for 3D visualization, are gradually replacing them.
Spine emergency MRI: To see the cord and soft tissue. Changes in cord signal and canal stenosis are important indicators.
Blood: protein electrophoresis, Ca2+, ESR, bone profile, FBC, and U&E.
Bence Jones protein in the urine is a sign of multiple myeloma.
Management
Traumatic cord injury: The ATLS recommendations should be followed while managing trauma injuries.
While it is debatable, NASCIS trial data suggests that giving high-dose steroids (methylprednisolone) to patients with severe spinal cord injuries for less than eight hours can improve their motor function.
Cord compression: If a tumor is found after imaging, high-dose steroids, such as dexamethasone, should be administered as away to lessen cord compression. Emergency radiation may potentially be effective in treating tumors. Get guidance from a neurosurgeon.
Surgery: Often required to remove the origin of compression and/or relieve compression.
External surgical stabilization: Using a halo or traction device, for instance.
Internal surgical stabilization: Using metal implants or bone grafts, for instance.
Surgical decompression: To relieve compression, a laminectomy, for instance.
For disc prolapses, a discectomy or microdiscectomy is used.
Rehabilitation: A multidisciplinary rehabilitation program including occupational therapy and physiotherapy, ideally in a specialized spinal unit.
Complications
Spinal function below the lesion is lost in cases of severe injury.
Paralysis of the breathing system: lesion above C4.
Quadriplegia, C4–T1.
Mid-thoracic: If above T6, paraplegia and autonomic dysreflexia.
S1: Loss of rectum and bladder control due to sacral parasympathetic loss.
Immobility-related complications include pressure sores, DVT, long-term spasticity (posing a risk of deformity), and heterotopic ossification.
Prognosis
When converted to the Frankel grade, the American Spinal Injury Association (ASIA) Impairment Scale after 72 hours after the injury has prognostic significance (see www.asia-spinalinjury.org for score sheet). Depending on the extent of the spinal cord injury, there may be some improvement over time.
