Surgery, Ortho and Emergency Flashcards
Scaphoid fractures - prognosis according to pole location
Distal pole fractures are 10% and proximal pole fracture are 20% of total scaphoid fractures.
Prognosis of distal pole fractures is better than proximal pole because of low risk of vascular compromise.
Fracture may take upto 1-2 weeks to become visible radiologically.
Most common site of fracture is waist of the bone and it is about 70% of total presentations.
CT scan is an investigation of choice for evaluation of union status in the scaphoid fracture.
organophosphate poisoning - Overview of the symptoms
Organophosphate poisoning acts on the cholinergic receptors and results in DUMBELS syndrome.
DUMBELS
–Diarrhoea
–Urination
–Miosis
–Bronchorrhea, bradycardia
–Emesis
–Lacrimation
–Salivation.
Most common causes of chronic liver disease and cirrhosis in Australia?
Alcoholic liver disease is the most common, followed by hepatitis C infection.
Hand innervation overview
In hand, ulnar nerve innervates all lnterosseous muscles, the 3rd and 4th lumbrical muscles, and muscles In the hypothenar eminence. While ulnar nerve injuries affect the function of these muscles, thenar eminence muscles are spared because they are supplied by the median nerve.
Low (distal) median nerve injuries affect the thenar muscles flexor pollicis brevis, abductor polllcis brevis and opponens pollicis.
Radial nerve supplies the muscles in the posterior compartment of the forearm, but no small muscle In the hand, thenar, or hypothenar eminences
Dual antiplatelet therapy prior to surgery? When to suspend?
Post-PCI (percutaneos coronary intervention)
< 1y - aspirin + clopidogrel sustained (avoid elective surgeries)
1-2y - continue aspirin and stop clopidogrel 5 days before
>2y - after that period, one’s only under use of aspirine, so can continue its use.
Fever and/or chills + jaundice + RUQ pain =?
Charcot’s triad
Fever and/or chills + jaundice + RUQ pain + hypotension + confusion =?
Reynold’s pentad
Suspicious malignant thyroid nodule - procedures?
< 1cm - lobectomy
1-4cm - total thyredectomy (consider RAI if T3, N1a, N1b)
> 4cm - total thyredectomy + LN ressection + radiotherapy
Thyroid tumors: most common and its overview
Papillary adenocarcinoma
Most common (70%) nodule in normal gland.
Presents with hoarseness and painless swelling
Mtx along lynphatics
Early adult life
Follicular Thyroid tumor - overview
Encapsulated - feels elastic on palpation
Mtx to lungs and bones from hematologic spread
After 40y.
15% incidence
Medullary Thyroid tumor - overview
After 50y
5% incidence
Hormone producing - endocrine dysfunction
Part of Multiple endocrine neoplasia
Mtx by lymphatics and bloodstream
Anaplastic Thyroid tumor - overview
Patients older than 60y
Hard irregular mass that grows quickly spreading by direct invasion to adjacent tissues
Painful and tender
Worst prognosis
Mallet finger - overview
Common in volley and basebal players
A flexion deformity of distant interphalangeal joint PREVENTING EXTENSION.
It results from rupture of the extensor tendon or avulsion fracture of distal phalanx
Intubation criteria
Hypoxemia - PO2 <60 mmHg on > 0.6 FIO2
Hypercarbia - PaCO2 > 60
RR > 30
GCS < 8
Hemodynamic instability - vasopressors
Open pneumothorax - immediate and definitive management
3-way wound dressing (avoid hipertensive pneumothorax)
chest tube insertion
Worst complication of supracondylar fracture?
Ischemia - presenting with absent pulse
= Exploration in the OR for reducing and stabilizing
Renal injury - overview (how to investigate, classification, management)
! If there’s urethral injury, there won’t be urine
If suspected = CT FOR EVALUATION
I - Contusion or Haematoma
II - Haematoma / Laceration (<1cm parenchymal depth of renal cortex with NO urinary extravasation)
III - Laceration (>1cm or with)
IV - Laceration (through the cortex, medula and collecting system)/ vascular injury
V - Laceration / vascular injury (complete mess)
I, II, III - non-operative management
IV - operative management if unstable
V - Nephrectomy
Management of Warfarin induced bleeding (High INR) - when to intervene?
> No bleeding:
If INR 5-8 = withold 1-2 doses warfarin and reduce maintenance dose
If INR > 8= give PO VITAMIN K 1-5mg
> Minor bleeding
Give VIT K IV 1-3mg
> Major bleeding = limb or life-threatening bleeding that requires reversal in 6-8H
Give VIT K IV 5mg + PCC - prothrombin complex concentrate (FFP - fresh frozen plasma - if PCC not available)
! Restart warfarin when INR < 5
! Repeat dose of VIT K if INR too high after 24h
Pre-menopausal Ovarian cysts - management - when to intervene?
(check for post-menopausal on fluxogram)
Pre-menopausal
< 5cm, simple, asymtomatic = reassurance
5-7cm, simple, asymp = repeat US IN 3-4 months
– if increase in size or symptomatic = refferal to OBGYN
> 7cm = symptomatic or complex in nature = refferal to OBGYN
= ALWAYS REFER IF SYMPTOMATIC
Investigation and management of hemorrhoids
- Symptoms include: bright red bleeding, pain, pruritus.
> If below the dentale line: External hemorrhoids (sometimes painful)
1 - Conservative treatment (lifestyle, stool softners, sitz baths)
> If internal (mostly painless)
- Not prolapsed (grade I) = 1
- Reduce at rest (Grade II) = 1
- Manually reducible (grade III) = non-surgical outpatien procedures.
Rubber band ligation
Sclerotherapy
Infrared coagulation
- Irreduceble prolapse, thrombosis (Grade IV) = surgical ttx
Arterial ligation
Hemorrhoidectomy
Hemorrhoidopexy
Indications for AAA repair
Male with AAA >5.5 cm
Female with AAA >5.0 cm
Rapid growth >1.0 cm/year
Symptomatic AAA (abdominal/back pain/tenderness, distal embolisation)
AAA Survaillance
Currently no formal AAA screening guidelines or programs exist in Australia,
(>50y with family history?)
3-3.9cm = 24 months
4-4.5 cm = 12 month
4.6-5.0cm = 6 months
>5.0 = 3 months
Suspected bowel obtruction - management
1 - CT OR XRAY
2- If signs of perforation or vascular compromise = LAPAROTOMY
3- If complete obstruction:
No oral intake, nasogastric intubation + rehydration EV
+
OBSERVE FOR 24-48H for resolution
4- If partial obstruction:
Same as above, but if no resolution: upper gastrointestinal/ small bowel follow through / enteroclysis -> if no resolution = laparotomy
Suggestive ALARM features of a gastrointestinal malignancy
New onset of dyspepsia in patient ≥60 years
-Evidence of gastrointestinal bleeding (hematemesis, melena, hematochezia, occult blood in stool)
-Iron deficiency anemia
-Anorexia
-Unexplained weight loss
-Dysphagia
-Odynophagia
-Persistent vomiting
-Gastrointestinal cancer in a first-degree relative
Atypical symptoms of GORD?
Chest pain, globus sensation, chronic cough, hoarseness, wheezing, and nausea
New onset of dyspesia - management
> 60y = Endoscopy
<60y with alarm signs = Endoscopy
without alarm features = Breath or
stool test for H. pylori
- Antimicrobial therapy: Amoxicilin 1g 2x/day + clarithromycin 500mg 2x/day + PPI for 14 days = TRIPLE THERAPY
If no improvement:
– Proton pump inhibitor for 4-8w
! Tests to confirm eradication should be performed in all patients treated for H. pylori. Eradication may be confirmed by a urea breath test, fecal antigen test, or upper endoscopy performed four weeks or more after completion of antibiotic therapy.
Severity of esophagitis classification
Los Angeles classification – grades esophagitis severity by the extent of mucosal abnormality, with complications recorded separately. In this grading scheme, a mucosal break refers to an area of slough adjacent to more normal mucosa in the squamous epithelium with or without overlying exudate.
-Grade A – One or more mucosal breaks each ≤5 mm in length
-Grade B – At least one mucosal break >5 mm long, but not continuous between the tops of adjacent mucosal folds
-Grade C – At least one mucosal break that is continuous between the tops of adjacent mucosal folds, but which is not circumferential
-Grade D – Mucosal break that involves at least three-fourths of the luminal circumference
Dysphagia - overview
Only for solids = mechanical obstruction:
> Nonprogressive = esophageal ring/eosinophilic esophagitis
> Progressive:
- Associated to chronic heartburn: Peptic stricture
- If elderly, significant weight loss and/or anemia: Esophageal/Cardia cancer
Solids and/or liquids = motor disorder:
> If progressive:
- Associated with heartburns: Scleroderma
- Regurgitation and/or RESPIRATORY SYMPTOMS and/or weight loss: Achalasia
!!! Might start with LIQUIDS ->SOLIDS
> If intermitent
Primary or secondary esophageal motility disorder
Progressive dysphagia to solids/liquids associated to regurgitation, weight loss and respiratory symptoms
Achalasia
Non progressive dysphagia only to solids?
Eosinphilic esophagitis
Progressive dysphagia only to solids associated with chronic heartburns?
Peptic stricture
Appendiceal carcinoid - management (appendicectomy or hemicolectomy?)
<=1CM = Appendicectomy
> 1cm <=2cm:
- Location at tip or mid appendix = appendicectomy
- Location at base, mesoappendiceal invasion; mtx = right hemicolectomy
> 2cm = right hemicolectomy
Peripheral artery disease - Screening?
Mesurement of ankle brachial index (ABI)
ABI testing is useful as a screening investigation for high-risk patients and as a first-line diagnostic test for symptomatic patients.
> > > The normal ABI range is 0.9–1.3.
For patients with symptoms of PAD and an abnormal ABI, further diagnostic imaging is indicated.
> Duplex ultrasonography is the first-line investigation, with stenosis >75% considered clinically significant.
Computed tomography angiography is a second-line investigation reserved for when concerns about aortoiliac disease arise following ultrasonography or for operative planning
PAD - Risk factor?
> > > > > > > SMOKING
hypertension, diabetes and hypercholesterolaemia,
Treatment recommendations for peripheral artery disease
> > > Smoking cessation: Recommended for all patients with PAD.
- Antithrombotic (antiplatelet or anticoagulant) therapy: Single-agent antiplatelet therapy (with aspirin 100–150 mg or clopidogrel 75 mg daily) is recommended for symptomatic patients, or following intervention.
Some patients may require dual antiplatelet therapy for a period (up to six months) after peripheral endovascular intervention or stenting.
Dual pathway inhibition with aspirin (100 mg daily) and low-dose rivaroxaban (2.5 mg twice daily) may be indicated for high-risk patients.
!! Anticoagulation (with warfarin or DOAC) IS NOT INDICATED for PAD treatment!!
For patients who require long-term
Ticagrelor is not indicated for treatment of PAD. - Antihypertensive therapy: Aim for blood pressure control of <140/80 mmHg in all patients with hypertension and PAD.
ACEIs or ARBs are considered first-line antihypertensive therapy in PAD.
Beta-blockers are not contraindicated but should be used with caution for patients with CLTI (chronic limb-threatening ischemia) - Lipid-lowering therapy: Statins are indicated for all patients with PAD, irrespective of serum cholesterol levels.
Lower LDL-C to <1.8 mmol/L or decrease by 50% if baseline is 1.8–3.5 mmol/L.
Prescribe the highest dose of statins tolerated to achieve LDL-C targets.
Combination therapy with ezetimide may be required.
Evidence for alternative, non-statin lipid-lowering agents is limited. - Glycaemic control: Aim for tight glycaemic control in patients with diabetes and PAD
!!Exercise caution when prescribing SGLT-2 inhibitors to patients with PAD because of the increased risk of amputation in some studies!!!
- Diet and exercise: Advice about healthy diet and physical activity is considered an essential part of PAD management.
Consider the addition of a multivitamin supplement if there are dietary insufficiencies or poor wound healing.
PE suspicion during pregnancy - initial and most apropriate diagnostic tests
CXR - Initial
US of the leg - Most appropriate
> If normal, with CXR normal - Low dose scintolography of the lungs
If normal, but CXR abnormal, CT Pulmonary Angiogram
Signs of bowel ischemia (eg. in volvulus)
Fever
Peritonitis
Leukocytosis
Jellyfish sting - management
Bluebottle and Minor jellyfish
AVOID VINEGAR
Wash sting site with seater and remove the tentacles
Hot water immersion (45º for 20 min)
Major box jellyfish and other box jellyfish
VINEGAR and remove tentacles
For MBJ - consider antivenom if cardiovascular collapse
Abdominal pain + metabolic acidosis
Mesentheric ischemia
Kidney stones - cutoff between ESPL and PCNL in most locations?
2 cm
(but in proximal ureteric stone = 1cm)
Variables measured in the Alvarado score for appendicitis
●Migratory right lower quadrant pain (1 point)
●Anorexia (1 point)
●Nausea or vomiting (1 point)
●Tenderness in the right lower quadrant (2 points)
●Rebound tenderness in the right lower quadrant (1 point)
●Fever >37.5°C (>99.5°F) (1 point)
●Leukocytosis of WBC count >10 x 109/L (2 points)
Score of 0 to 3 indicates appendicitis is unlikely and other diagnoses should be pursued. Score of ≥4 indicates that the patient should be further evaluated for appendicitis.
Bariatric sugery - what syndrome causes bilious vomit?
Efferent loop syndrome
Bariatric sugery - what syndrome causes non-bilious vomit?
Afferent loop syndrome
How will you determine worse prognosis of Laparoscopic appendicectomy?
Retrocecal peritonitis
Latex hypersensitivity - Risk Factors?
Patients with a history of asthma, dermatitis, or eczema.
Patients with food allergy, especially to avocado, kiwi, banana, mango, melon, pineapple, chestnut, or hazelnut.
> > > Patients exposed to repeated bladder catheterization»_space;» Eg. TSPINA BIFIDA
Patients with a history of anaphylaxis of uncertain etiology.
Healthcare workers who frequently wear latex gloves.
Workers with occupational exposure to latex (e.g., hairdressers, greenhouse workers, latex glove manufacturers, housekeeping personnel, and textile workers).
The identification of patients at risk for a latex allergy is an essential step before medical procedures that involve latex exposure occur.
Tension pneumothorax - features
The classic presentation of tension pneumothorax includes distended neck vein, hypotension, diminished or absent breath sounds and tracheal deviation to the other side
“Patients with asymptomatic gallstones become symptomatic at a rate of about 2 percent per year” - T OR F?
TRUE
Lynch syndrome (hereditary nonpolyposis colorectal cancer) - dominant or recessive? Survaillance screen? Cancer prevention?
is an autosomal dominant condition caused by germline mutations in any one of the mismatch repair genes (MSH2, MLH1, MSH6, PMS2) ) or a deletion of the last few exons of the gene EPCAM that results in epigenetic silencing of MSH2
Surveillance colonoscopy every 1 to 2 years is recommended for individuals carrying a germline mutation or clinically at risk of carrying a mutation but in whom definitive testing is not possible. It should commence at age 25 or 5 years younger than the youngest affected family member if < 30 years. Annual surveillance is preferred in known mutation carriers. The risk of colorectal cancer is lower and the age of diagnosis is later in carriers of MSH6 or PMS2 mutations and surveillance starting at age 30 years could be considered.
Aspirin at 600 mg/day reduced Lynch syndrome cancer incidence by 50–68% in the Colorectal Adenoma/Carcinoma Prevention Programme 2 (CAPP2) trial. Follow-up of the low-dose aspirin randomised controlled trials (RCTs) suggests low-dose aspirin (100 mg/day) also reduces cancer incidence by half.
Reference:
1/ https://www.racgp.org.au/clinical-resources/clinical-guidelines/key-racgp-guidelines/view-all-racgp-guidelines/genomics-in-general-practice/familial-colorectal-cancer/
2/ https://lynchsyndrome.org.au/
3/ https://www.racgp.org.au/clinical-resources/clinical-guidelines/key-racgp-guidelines/view-all-racgp-guidelines/red-book/early-detection-of-cancers/colorectal-cancer
Supraclavicular limphonodes - meaning
The left supraclavicular lymph node takes its supply from lymph vessels in the abdominal cavity. The finding of an enlarged, hard node has long been regarded as strongly indicative of the presence of cancer in the abdomen, specifically gastric cancer, that has spread through the lymph vessels.
An enlarged right supraclavicular lymph node tends to drain thoracic malignancies such as lung and esophageal cancer, as well as Hodgkin’s lymphoma.
Hemorrhage classification
Class I Hemorrhage means up to 15% of blood volume lost (up to 750 mL).Pulse rate less than 100, systolic blood pressure normal, respiratory rate is 14 to 20, urine output is greater than 30 mL/hour, mental status is slightly anxious.
Class II Hemorrhage means from 15% to 30% blood volume loss (750 mL to 1500 mL).Pulse rate is from 100 to 120, systolic blood pressure normal, respiratory rate is 20 to 30, urine output is 20 to 30 mL/hour, mental status is mildly anxious.
Class III Hemorrhage means from 30% to 40% blood volume loss (1500 mL to 2000 mL).Pulse rate is from 120 to 140, systolic blood pressure is decreased, respiratory rate is 30 to 40, urine output is 5 to 15 mL/hr, mental status is anxious and confused. This patient is suffering from class lll hemorrhagic shock.
Class IV Hemorrhage means blood loss of greater than 40% (greater than 2000 mL). The pulse rate is greater than 140, systolic blood pressure is decreased, the respiratory rate is greater than 35, urine output is negligible, mental status is confused and lethargic.
When is Metabolic or bariatric surgery indicated?
– BMI above 40 with no co-morbidities
– BMI above 35 with co-morbidities such as hypertension
– BMI above 30 with poorly controlled type 2 diabetes
– BMI above 30 with increased cardiovascular risk due to multiple risk factors such as hypertension, hyperlipidemia, strong family history of cardiovascular disease at a young age.
Abdominal disconfort + growth delay + microcytic anaemia, suspicion?
Celiac disease
Celiac disease - Diagnosis?
Serologically (eg, antitissue transglutaminase antibody, anti-endomysial antibody) or by duodenal biopsy (eg, intraepithelial lymphocytosis, villous blunting).
Management includes a gluten-free diet.
Child pugh - Overview
The Child-Pugh system is used to assess the prognosis of patients with liver disease and cirrhosis by calculating 1-year survival rate. This system takes into account the following 5 parameters for determination of the prognosis:
The presence of ascites
Bilirubin level
Albumin level
Prothrombin time
Encephalopathy
Class A (scores 5-6): well -compensated disease – one- and two-year survival are 100%and 85% respectively.
Class B (scores 7-9): functional compromise – one- and two-year survival are 80% and 60%
Class C(scores 10-15): decompensated disease – one- and two -year survival are 45% and 35% respectively.
Caustic ingestion - overview
Mucosal injury results from contact with the caustic substance (rather than from systemic absorption); therefore, patients often have immediate oropharyngeal, retrosternal, or epigastric pain as well as dysphagia and hypersalivation (eg, drooling). Vomiting and hematemesis may also occur. Patients should initially undergo assessment and stabilization of the airway, breathing, and circulation. Serial chest and abdominal x-rays should be obtained to identify any signs of perforation, such as pneumomediastinum, pleural effusions, or subdiaphragmatic air (none of which are seen in this patient). An upper gastrointestinal x-ray study with water-soluble contrast should be performed in patients with suspected perforation.
The severity of esophageal injury cannot be predicted by either clinical symptoms or the extent of oral injury seen on physical examination.
> > In the absence of perforation or severe respiratory distress, endoscopic evaluation within the first 24 hours is recommended to assess the severity of esophageal damage.
Activated charcoal can decrease the systemic absorption of poisons; however, caustic ingestions cause immediate local damage on contact with the esophagus. In addition, charcoal would obstruct the view during endoscopy.
Caustic ingestion - overview (fluxogram)
Chemical burn or liquefaction necrosis resulting in:
Laryngeal damage: hoarseness, stridor
Esophageal damage: dysphagia, odynophagia
Gastric damage: epigastric pain, bleeding
Management
Secure airway, breathing, circulation
Decontamination: remove contaminated clothing & visible chemicals; irrigate exposed skin
Chest x-ray if respiratory symptoms
Endoscopy within 24 hr
Complications
Upper airway compromise
Perforation
Strictures/stenosis (2-3 weeks)
Ulcers
Cancer
Heat exhaustion - overview
Heat exhaustion typically occurs after prolonged exercise (eg, soccer) in high ambient temperatures, particularly in the setting of high humidity, which limits evaporative cooling from sweat
Risk factors
Strenuous activity during hot & humid weather
Dehydration, poor acclimatization
Lack of physical fitness, obesity
Acute illness (common in diseases like cystic fibrosis)
Medications: anticholinergics, antihistamines, phenothiazines, tricyclics, antipsychotics
Manifestations
Hyperthermia ≤40 C WITH NORMAL MENTAL SATUS
Profuse sweating
Nausea/vomiting
Headache, dizziness
Tachycardia, hypotension
Management
Cool patient (eg, air conditioning, cool water shower)
Salt-containing oral fluids
Cholangitis - management
Plan for immediate decompression if the patient does not respond to initial measures
Plan for biliary decompression on semi-urgent basis (<72 hours) if the patient is responding to initial resuscitation
Plan for urgent decompression (within 24-48hrs) if the patient is older than 70 years
The most appropriate method of biliary decompression is ERCP, sphincterectomy and stenting
Acute ascending cholangitis is initially managed with aggressive fluid resuscitation and intravenous antibiotics fol lowed by biliary decompression.
Since the infectious organisms responsible for acute ascending cholangitis are enteric gram negative bacteria, the selected antibiotic of choice should provide appropriate coverage against these germs.
All patients with ascending cholangitis require biliary drainage. In about 85-90% of patients, there is respond to medical therapy. In this group decompression may be per formed semi-electively during the same admission (and ideally within 72 hours); however for the following patients urgent decompression may be considered:
Patients older than 70 years
Patients with diabetes
Patients with other comorbid conditions
Approximately 10% to 15% of patients (not the majority) fail to respond within 12 to 24 hours or deteriorate after initial medical therapy and need urgent biliary decompression. Delay t o do so increases the chance of an adverse outcomes.
Necrotizing enterocolitis - Overview
infant has bilious emesis, abdominal distension, leukocytosis, and metabolic acidosis due to necrotizing enterocolitis (NEC). Pathogenesis of NEC involves inflammation and necrosis of intestinal mucosa with invasion of gas-producing bacteria. Premature and very low-birth-weight (<1.5 kg [3.3 lb]) infants are particularly vulnerable due to decreased bowel motility, increased intestinal permeability, and immature host defenses. Exposure to bacteria from enteral feeds, especially formula feeds, also increases the risk of NEC.
Initial signs are often nonspecific (eg, lethargy, feeding intolerance), and neonates may be hypothermic (<36.5 C [97.7 F]) rather than febrile, as seen here. Bilious emesis and a tense, erythematous, distended abdomen are typical. Bloody stools are also a classic finding but may not be present in early stages. Leukocytosis and metabolic acidosis reflect inflammation and intestinal ischemia, respectively.
The hallmark x-ray finding in NEC is air in the bowel wall, or pneumatosis intestinalis (red arrows). In addition, portal venous air (yellow arrows) is seen as branching areas of lucency over the liver due to gas-producing bacteria and the transmigration of gas from the bowel wall to the mesenteric and portal veins. Severe intestinal necrosis can also cause perforation and pneumoperitoneum.
Management of suspected NEC includes discontinuation of enteral feeds and administration of antibiotics; surgery may be required in severe cases.
Necrotizing enterocolitis - overview (fluxogram)
Bilious emesis and abdominal distension in a preterm neonate are highly suggestive of necrotizing enterocolitis. Abdominal x-ray findings include pneumatosis intestinalis (intramural air) and portal venous air.
Pathogenesis
Gut mucosal wall invasion by gas-producing bacteria
Intestinal inflammation, necrosis
Risk
factors
Prematurity
Very low birth weight (<1.5 kg [3.3 lb])
Enteral feeding
Clinical findings
Nonspecific: apnea, lethargy, vital sign instability
Gastrointestinal
Abdominal distension
Feeding intolerance, bilious emesis
Bloody stools
X-ray findings
Pneumatosis intestinalis (air in bowel wall)
Pneumoperitoneum (free air under diaphragm)
Complications
Sepsis, disseminated intravascular coagulation
Late: strictures, short-bowel syndrome
Management of suspected NEC includes discontinuation of enteral feeds and administration of antibiotics; surgery may be required in severe cases.
Pyloric stenosis, Duodenal atresia and Hirschprung’s - presentation
Pyloric stenosis presents with postprandial nonbilious emesis in an otherwise healthy 3- to 6-week-old infant. An olive-shaped abdominal mass may be palpable, and metabolic alkalosis is expected.
Duodenal atresia, characterized by the double bubble sign (dilated stomach and duodenum) on x-ray, presents with bilious vomiting after initiation of feeds. Patients do not have yellow, seedy stools (as this infant does) because feeds cannot pass through the duodenum.
Hirschsprung disease causes abdominal distension, feeding intolerance, and failure to pass meconium within 48 hours of birth. Milder disease may be diagnosed later in life, but patients typically have a history of chronic constipation and poor weight gain.
Rectal prolapse - overview
Rectal prolapse
Risk factors
Women age >40 with history of vaginal deliveries/multiparity
Prior pelvic surgery
Chronic constipation, diarrhea, or straining
Stroke, dementia
Pelvic floor dysfunction or anatomic defects
Clinical presentation
Abdominal discomfort - NOT PAIN
Straining or incomplete bowel evacuation, fecal incontinence
Digital maneuvers possibly required for defecation
Erythematous mass extending through anus with concentric rings (full-thickness prolapse) or radial invaginations (non–full-thickness prolapse)
Management
Medical
Considered for non–full-thickness prolapse
Adequate fiber & fluid intake, pelvic floor muscle exercises
Possible biofeedback therapy for fecal incontinence
Surgical
Preferred for full-thickness or debilitating symptoms (eg, fecal incontinence, constipation, sensation of mass)
Clinical features of irritable bowel syndrome
Recurrent abdominal pain/discomfort ≥1 day/week for past 3 months & ≥2 of the following:
Rome IV diagnostic criteria
Related to defecation (improves or worsens)
Change in stool frequency
Change in stool form
Alarm features
Older age of onset (≥50)
Gastrointestinal bleeding
Nocturnal diarrhea
Worsening pain
Unintended weight loss
Iron deficiency anemia
Elevated C-reactive protein
Positive fecal lactoferrin or calprotectin
Family history of early colon cancer or IBD
Bilious emesis in neonates - overview
View image
Initial management of clinically stable patients (eg, normal vital signs) with bilious emesis includes cessation of enteral feeds, nasogastric tube decompression, administration of intravenous fluids, and diagnostic imaging. In patients with volvulus, an x-ray may identify dilated loops of bowel and air-fluid levels (due to intestinal obstruction) or pneumoperitoneum (due to intestinal perforation). However, x-rays may be normal and are insensitive for midgut volvulus; serial x-rays are unlikely to be diagnostic.
Therefore, all hemodynamically stable infants with bilious emesis and a nondiagnostic x-ray, as seen in this patient, warrant an upper gastrointestinal (GI) series to evaluate for midgut volvulus. Diagnostic findings include an abnormally located ligament of Treitz on the right side of the abdomen (malrotation) and a duodenal corkscrew, or bird’s-beak, appearance (volvulus).
A contrast enema is indicated for distal bowel obstructions, such as Hirschsprung disease and meconium ileus (microcolon). Bilious emesis can occur; however, these conditions usually present with failure to pass meconium within the first 2 days of life and dilated loops of bowel on x-ray.
CT scan of the abdomen with intravenous contrast may identify midgut volvulus. However, an upper GI series is preferred for the evaluation of malrotation because it is more sensitive and has less radiation exposure.
Pyloric stenosis, diagnosed by a hypertrophied pyloric muscle on ultrasound, typically presents at age 3-5 weeks with projectile vomiting, which is nonbilious due to gastric outlet obstruction. In addition, classic findings include visible peristaltic waves and a palpable abdominal mass, neither of which is seen in this patient
The gold standard for volvulus diagnosis is an upper gastrointestinal series, which shows a right-sided ligament of Treitz and a corkscrew duodenum.
GORD - Indication for endoscopy
Indication for endoscopy
Persistent symptoms despite an adequate trial of proton pump inhibitor therapy
Treatment of complications such as dilatation of oesophageal strictures
Evaluation of patients before and after anti-reflux surgical procedures
Screening for Barrett’s oesophagus in high-risk patients (may be considered, e.g. in overweight men over 50 years, however evidence that screening improves outcomes is lacking)
Eosinophilic oesophagitis should be considered in patients, particularly men, in their 20s and 30s with a history of food allergy or atopy who present with dysphagia or refractory symptoms suggestive of GORD.
Biopsy may be needed to exclude eosinophilic oesophagitis. There is no evidence that routine screening for
Barrett’s oesophagus improves mortality or is cost-effective. However, it may have a role in high-risk groups such as the overweight and Caucasian males over 50 years old with no previous endoscopic investigation.
In the absence of alarm symptoms, a therapeutic trial is generally favored over more expensive diagnostic studies (endoscopy, CT scan). Classic symptoms of GORD do not mandate an evaluation for coronary artery disease unless other features suggest this diagnosis.
Red Flags in GORD which require further evaluation:
Red Flags in GORD which require further evaluation:
Recurrent vomiting
Dysphagia or odynophagia
Weight loss
Evidence of gastrointestinal blood loss e.g. haematemesis, iron deficiency or anaemia
Duration of symptoms >5 years or <6 months
Epigastric mass
Age >50 years
www.racgp.org.au/afpbackissues/2004/200411/20041128piterman.pdf
Barrett ‘s esophagus is the most significant risk factor for development of which neoplasm?
Oesophageal adenocarcinoma.
Pancreatic pseudocysts - overview and management
Pancreatitis pseudocysts are diagnoses with CT or ultrasound scan. Where the diagnosis is in doubt, the content can be aspirated (under endoscopic ultrasonography or CT scan) and examined.
Surgical intervention should be considered if any of the following is present:
Compression of large vessels (clinical symptoms or seen on CT scan)
Gastric or duodenal outlet obstruction
Stenosis of the common bile duct due to compression
lnfected pancreatic pseudocysts
Hemorrhage into pancreatic pseudo cyst
Pancreatico-pleural fistula
There are two main types of endoscopic drainage:
Transmural drainage: in this method, using endoscopy, a small incision is made in the stomach (endoscopic cystgastrostomy [ECG]) or in duodenum (endoscopic cystduodenostomy [ECO]) to let the pseudocyst drain into the stomach or duodenum. ECO is preferred over ECG
Transpapillary drainage: this method is safer and more effective than transmural drainage, but requires that the cyst communicates with the pancreatic duct because this method includes entering the pancreatic duct by ERCP, and from there,into the pseudocyst. Stents may be left in place to facilitated drainage.
Generally, endoscopic drainage methods are preferred over open surgical treatment if eligibility is met and there is no contraindication because these methods are less invasive and associated with fewer complications.
Laparotomy with cyst excision and internal and external drainage is still the gold standard management option; however it is ONLY considered first -line therapy for surgical Intervention in the following conditions:
Complicated pseudocysts i.e. infected or necrotic
Pseudocysts associated with pancreatic duct stricture and a dilated pancreatic duct
Suspected cystic neoplasia
Presence of pseudoaneurysm, unless it has been embolised before the procedure
Coexistence pseudocysts and bile duct stenosis
Complications such as compression of the stomach or the duodenum, perforation or pseudoaneursyms
Endoscopic cystgastrostomy (ECG) or duodenostomy (ECO) are methods of choice if the pseudocyst is not communicating with the pancreatic duct.
Laparotomy and surgical removal of the cyst is considered if endoscopic methods fail or there is a contraindication.
Percutaneous catheter drainage has low success rate and high recurrent rates. It is never considered for treatment of a pancreatic pseudocyst. However, in infected pseudo cysts it is the procedure of choice for sampling and examining the material as the most appropriate initial step.
Conservative management is not an appropriate option for symptomatic pseudocysts.
Dumping syndrome - definition
Dumping syndrome is a condition in which food, especially food high in sugar, moves from your stomach into your small bowel too quickly after you eat. Sometimes called rapid gastric emptying, dumping syndrome most often occurs as a result of surgery on your stomach or esophagus.
Dumping syndrome - Overview of types and management
Early dumping
Symptoms of early dumping syndrome occur 30-60 minutes after a meal and are believed to result from accelerated gastric emptying of hyperosmolar contents in to the small bowel.
This leads to fluid shift from the intravascular compartment in to the bowel lumen resulting in rapid small bowel distention and increase in the frequency of bowel contractions. Even in healthy persons without gastric surgery, rapid instillation of liquid meals into the small bowel has shown to induce dumping syndrome
Rapid shift of fluid into the intestinal lumen results in decreased circulating volume,triggering a vasomotor response presenting with tachycardia and lightheadedness.
Late dumping
Late dumping occurs 1-3 hours after a meal.
The pathogenesis is though to be related to the early development of hyperinsulinemic {reactive) hypoglycemia.
Rapid delivery of a meal to the small intestine results in an initial high concentration of carbohydrates in the proximal small bowel and rapid absorption of glucose.This is replied by a hyperinsulinemic response. The high insulin levels stay for longer period and are responsible for the subsequent hypoglycemia.
Supplementation with dietary fiber has proven effective in the treatment of hypoglycemic episodes . Many medical therapies have been tested, including pectin, guargum. and glucomannan. These dietary fibers form gels with carbohydrates, resulting in delayed glucose absorption and prolongation of bowel transit time
Dietary change to a low-carbohydrate, high protein diet, as well as the use of alpha-glucosidase inhibitors, may be useful to control the symptoms of dumping. This is preferential to subtotal or total pancreatectomy in those persons with severe symptoms
Most patients have relatively mild symptoms and respond well to dietary changes.
In some patients with postprandial hypotension,lying supine for 30 minutes after meals may delay gastric emptying and also increase venous return thereby minimizing the chances of syncope.
Colorectal screening intervals
Perform immunochemical fecal occult blood test (iFOBT) every 2 years from 50 – 74 years of age.
Major head trauma followed by headaches, nausea, vomiting and sleepness in rural area - Management
Facing Major Deterioration:
- Tranfer time >2h
IOT, Mannitol, Moderate hyperventilation, Burr hole evacuation or craniectomy/otomy
and then RETRIEVAL - Tranfer time < 2h
IOT, Mannitol, Moderate hyperventilation,
Four-month by brought by his mother with episodic swelling on the left side; the spermatic cord is the thicker on palpation. On examination, no inguinoscrotal swelling is palpable with a soft abdomen. What is the diagnosis?
Inguinal Hernia
SILK GLOVE SIGN:
Index finger is lightly rubbed over the cord from side to side over the pubic tubercle - cord structures are thickened (feels like two silk sheets rubbing against one another, reflecting the smooth peritoneal sac edges),
Sensitivity = 93%, specificity = 97%
Difference between spontaneous primary and secondary pneumothorax?
Primary - otherwise healthy person
Secondary - evidence of underlying lung disease (>50a + smoking history)
Spontaneous primary and secondary pneumothorax - management
Primary:
> 2cm and/or breathless:
Aspirate with 16-18G cannula and review in 2-4weeks
< 2cm:
Review in 2-4weeks
Secondary:
> 2cm or breathless:
Chest drain 8-14fr and Admit
1-2cm:
Aspirate with 16-18G cannula (<2,5l) and review in 2-4weeks
If succes and size <1cm - Admit, high flow O2,observe 24h
If no success = Chest drain
<1cm
Admit, high flow O2,observe 24h
Prostatic carcinoma treatment according to PSA levef
PSA > 20 or distant Metastatic - Androgen deprivation therapy or orchiectomy.
PSA > 20 and spinal Metastasis - androgen deprivation therapy or radiotherapy of the spine.
Locally advanced T3b (seminal vesicle or capsule) - External beam radiotherapy for prostate cancer (EBRT) + ADT
PSA < 10, without comorbidity, and foci found in Biopsy <10% or one out of 12 - active surveillance
PSA even doubled, life expectancy <10 years - watchful waiting
PSA doubled but under 10, foci <10% with lower urinary tract symptoms - radical prostatectomy
Prostatic carcinoma staging
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