Surgery - General Flashcards
What are the most common causes of small and large bowel obstruction?
- Most common small bowel causes = adhesions, hernia
- Most common large bowel causes = malignancy, diverticular disease, volvulus
How does bowel obstruction present?
- Presentation
- Abdo pain (colicky or crampy)
- Vomiting (early in proximal, late in distal)
- Abdo distension
- Absolute constipation (early in distal, late in proximal)
- O/E
- Surgical scars (adhesions etc), hernia, abdo distension
- Assess fluid status
- Tympanic on percussion
- Tinkling bowel sounds on auscultation
- Abdo tenderness (but if there is guarding/rebound tenderness then suspect ischaemia!!! Do vbg for lactate)
How would you investigate and manage bowel obstruction?
- Investigations
- Definitive = ct abdo pelvis with iv contrast
- Differentiates between pseudo-obstruction and mechanical too
-
AXR
- S bowel = dilated >3cm, central, valvulae conniventes (lines totally across bowel)
- L bowel = dilated >6cm or >9cm in caecum, peripheral, haustra visible (incomplete lines across bowel)
- In perforation you can see Riglers sign (both sides of bowel visible) or psoas sign (loss of sharp delineation of psoas muscle border)
- Erect CXR if suspected bowel perf = pneumoperitoneum
- Definitive = ct abdo pelvis with iv contrast
- Management
- Conservative = “drip and suck”
- NBM + NG tube to decompress bowel
- IV fluids and correct electrolytes
- Urinary catheter, fluids
- Analgesia, anti-emetics
- Adhesions = usually conservative unless strangulated/ischaemic
- Do water soluble contrast study if not resolved in 24 hours
- If contrast does not reach colon in 6 hours then take to theatre as it is unlikely to resolve
- Conservative = “drip and suck”
- Surgical = generally a laparotomy, sometimes resection + stoma
- For ischaemia or closed loop bowel obstruction
- Or if patients treated conservatively don’t improve
What two ways does an upper GI bleed present as?
Melena (black tarry offensive smelling stools)
Haematemesis (vomiting blood)
What are some differentials for an upper GI bleed?
-
Peptic ulcer disease
- Most signif bleeding if ulcer erodes through posterior gastric wall into gastroduodenal artery (also common in lesser curve of stomach)
- Suspect in nsaids or steroids, dyspepsia like hx, h pylori positive
-
Variceal bleeds
- Commonly Oesophageal varices due to alcoholic liver disease
- Upper gi malignancy
-
oesophagitis
- inflammation of intraluminal epithelial layer of the oesophagus
- due to GORD (most common), or infections (candida albicans), meds (bisphosphonates), radiotherapy, crohns
-
Mallory Weiss tear
- Recurrent vomiting then haematemesis
- Forceful vomiting causes a tear in the epithelial lining of the oesophagus
- Meckels diverticulum
- Vascular malformations eg. dieulafoy lesion
How would you investigate an upper GI bleed generally?
+ scoring systems
- Investigations
- Oesophagogastroduodenoscopy is definitive
- CT abdo with iv contrast to assess any active bleeding
- Fbc, u&es, lfts, clotting, group and save, abg
- Erect cxr if perforated peptic ulcer suspected
- Glasgow-Blatchford Bleeding score for upper gi bleeds
- Rockall severity score for GI bleeding post endoscopy
- AIMS65 score for risk of in-hospital mortality from upper gi bleed
How would you manage an upper GI bleed generally?
(peptic ulcer and varices too)
- Peptic ulcer
- During OGD, give adrenaline injection** and **cauterise bleeding.
- High dose ppi eg. iv 40mg omeprazole
- Active bleeding can be treated with angio-embolisation
- Oesophageal varices
- Endoscopic banding
- Prophylactic antibiotics
- Somatostatin analogues (eg. octreotide) or vasopressors (eg terlipressin) to reduce splanchnic blood flow
- Sengstaken-Blakemore tube for uncontrollable/severe
- Longterm = repeated banding and long term BB
- Blood products for hb<70g/L
- FFP+/- platelets for impaired liver function
- Reversal agents for anticoagulants
What are some differentials for a lower GI bleed?
-
Diverticular disease
- Outpouchings of bowel wall consisting of mucosa
- Commonly in descending and sigmoid colon
- Diverticular disease bleeds are painless
- Diverticulitis bleeds are painful
- Ischaemic/infective colitis
-
Haemorrhoids
- Engorged vascular cushions in anal canal
- Blood on surface of stool not mixed
-
Malignancy
- In elderly, always suspect colorectal cancer
- Angiodysplasia
- Crohns
- UC
- Radiation proctitis
How would you investigate and manage a lower GI bleed? and scoring systems
Investigations
- Oakland score (stratifies if pt with lower gi bleed can be managed as outpatient)
- Fbc,u&es, lfts, clotting, group and save, stool cultures
- Urgent ct angiogram for haemodynamically unstable (can embolise during)
-
Flexi sigmoidoscopy
- Full colonoscopy if nothing on flexi sig
- OGD if nothing on colonoscopy
- Capsule endoscopy or mri small bowel can also be done
Management
- A-e resus
- Packed rbc for hb<70, reverse anticoagulation
- Endoscopic haemostasis methods eg. adrenaline injection
- surgical
What are risk factors of GORD?
- male, old age, obesity, alcohol, smoking, caffeine, spicy food
How dose GORD present?
-
Burning retrosternal chest pain (worse after meals, lying down, bending over, straining)
- Relieved by antacids
- Excessive burping
- Odynophagia
- chronic/nocturnal cough
How would you investigate and manage GORD?
Investigations
- Los Angeles classification of reflux oesophagitis
-
OGD to rule out red flags for upper gi malignancy
- Dysphagia
- >55 with weight loss, upper abdo pain, dyspepsia, reflux
- OGD also investigates oesophagitis, structuring, barretts
- Gold standard for GORD = 24 hour pH monitoring
- Oesophageal manometry to rule out oesophageal dysmotility
Management
- Conservative
- Avoid alcohol, coffee, fatty foods
- Weight loss
- Smoking cessation
- PPIs
- Surgical
- Fundoplication (se = bloating, dysphagia, inability to vomit)
What are the two kinds of oesophageal cancer?
How would they present?
Squamous cell = middle and upper 1/3 of oesophagus
- Risk factors = smoking, alcohol, low vit a, chronic achalasia
Adenocarcinoma = lower 1/3 of oesophagus
- Risk factors = barretts (metaplastic epithelium that progresses to dysplasia), GORD, obesity, high fat intake
Presentation
- Progressive dysphagia (solids first)
- Weight loss, cachexia, supraclavicular lymphadenopathy
- Odynophagia
How would you investigate and manage oesophageal cancer?
Investigations
-
Urgent OGD in 2weeks
- Biopsy and send to histology
- CT CAP and PET CT for mets
- Endoscopic US to assess penetration into oesophageal wall (T stage)
- Staging laparoscopy for intraperitoneal mets
- Fine needle aspiration of palpable cervical lymph nodes
- Bronchoscopy for hoarseness or haemoptysis
Management
- Definitive
- SCC = difficult to operate on so usually chemoradiotherapy
- Adenocarcinoma = neoadjuvant chemo or chemoradiotherapy, followed by oesophageal resection
- Most will need a feeding jejunostomy after surgery to aid nutrition
- Surgery risks = anastomotic leak, pneumonia etc
- Palliative
- Oesophageal stent for difficulty swallowing
- Radiotherapy/chemotherapy to reduce tumour size/bleeding
- Nutritional support = thickened fluid and nutritional supplements
- Radiological inserted gastrostomy (RIG) tube insertion for severe dysphagia
Oesophageal tears:
Boerhaave’s Syndrome is full thickness, Mallory Weiss is lacerations of the mucosa.
How does Boerhaave’s present?
- Stomach contents leak into mediastinum and pleural cavity
- Severe inflammatory response and multi organ failure
- Causes = iatrogenic like endoscopy or forceful vomiting
- Presentation
- Severe sudden onset retrosternal chest pain, resp distress, subcutaneous emphysema
- Hx of severe vomiting and retching
- Mackler’s triad = vomiting, chest pain, subcut emph
How would you investigate and manage Boerhaaves?
Investigations
- Fbc, u&es, lfts, clotting
- Definitive = urgent ct abdo pelvis with iv and oral contrast
- Cxr for pneumomediastinum or intrathoracic air fluid levels
- If high clinical suspicion, just do urgent endoscopy in theatre
Management
- A-e resus
- Surgical
- Endoscopy to determine site of perf
- Thoracotomy to Control leak and wash out chest
- Do a contrast ct at 10 days before starting oral intake as leaking is common
- Insert feeding jejunostomy in surgery for nutrition
- Non operative (iatrogenic perfs usually more suitable as they are more stable)
- Resus and transfer to icu/hdu
- Antibiotics and antifungal cover
- NBM for 1-2 weeks, ng tube insertion on drainage
- Large bore chest drain insertion
- TPN or feeding jejunostomy insertion
How would a Mallory Weiss tear present?
- Typically at gastro-oeosphgeal junction
- Presentation
- Hx of profuse vomiting then short period of haematemesis
- Usually fine unless clotting abnormalities or anti-coag drugs
What is Achalasia? How would it present?
Achalasia = failure of LOS to relax, progressive failure of contraction of proximal oesophageal smooth muscle
- Due to progressive destruction of ganglion cells in the myenteric plexus
Presentation
- Progressive dysphagia with solids and liquids
- Regurgitation
- Coughing especially at night
- Chest pain
- Weight loss
How would you investigate and manage Achalasia?
Investigations
- Barium swallow
-
oesophageal manometry is gold standard for motility disorders
- shows absence of oesophageal peristalsis, failure of relaxation of LOS, high resting LOS tone
- urgent OGD to rule out oesophageal cancer
Management
- Conservative
- Sleeping on pillows
- Eating slowly
- Chewing food thoroughly
- More fluids with meals
- CCB or nitrates (temporary)
- Botox injections in LOS by endoscopy (temporary)
- Surgical
- Endoscopic balloon dilation
- Laparoscopic heller myotomy
What is diffuse oesophageal spasm?
How would it present
Diffuse oesophageal spasm = multi focal high amplitude contractions of the oesophagus
- Due to dysfunction of oesophageal inhibitory nerves
Presentation
- Severe dysphagia to solid and liquids
- Central chest pain exacerbated by food
- Responds to nitrates
How would you investigate and manage diffuse oesophageal spasm?
Investigations
- Manometry shows repetitive, simultaneous and ineffective contractions of the oesophagus
- Barium swallow can show corkscrew appearance
Management
- Nitrates or CCB to relax smooth muscle
- Pneumatic dilation
- Myotomy for severe
What is a hiatus hernia and what are the two types?
Hernia = Protrusion of a whole or part of an organ through the wall of the cavity that contains it into an abnormal position
Hiatus hernia = protrusion of an organ from the abdo cavity into the thorax through the oesophageal hiatus (usually stomach)
- They can be classified into sliding or rolling
- Sliding = Gastro-oesophageal junction + abdo part of oesophagus + cardia of stomach slides up through diaphragmatic hiatus into the thorax
- Rolling = upward moving of gastric fundus so it lies beside a normal GOJ, resulting in a “bubble” of stomach in the thorax
What are some risk factors of a hiatus hernia?
- old age (loss of diaphgragmatic tone), increased abdo pressure (eg. coughing, obesity, pregnancy, ascites)
How would a hiatus hernia present?
- Mainly asymptomatic
- Reflux eg. burning epigastric pain worse on lying flat
- Hiccups or palpitations (large hernias can irritate diaphragm or pericardial sac)
- Swallowing difficulties (oesophageal stricture formation)
- Vomiting and weightloss
- Bleeding/anaemia (oesophageal ulceration)
How would you investigate and manage a hiatus hernia?
Investigations
- OGD is gold standard
Management
- PPI like omeprazole
- Weight loss, smaller meal portions with low fat content, sleeping with head of bed raised
- Smoking cessation, reduce alcohol
- Surgery like cruroplasty or fundoplication
What are some complications of a hiatus hernia?
- Rolling ones are prone to incarceration and strangulation
-
Gastric volvulus can occur and cause obstruction and tissue necrosis
- Borchardt’s triad of severe epigastric pain, retching without vomiting, inability to pass an NG tube
What is peptic ulcer disease?
- A break in the lining of the GI tract extending through to the muscularis mucosae
- Most commonly in the lesser curvature of the proximal stomach or the first part of the duodenum
- Normal protective mechanisms = hco3- ions and mucous secretion by the gi mucosa
What are some risk factors of peptic ulcer disease?
- Hpylori, Nsaids, corticosteroids, physiological stress, head trauma, Zollinger Ellison syndrome
- Hpylori
- Produces urease to break down urea into co2 and ammonia (neutralises stomach acid to create an alkaline environment)
- Sets off inflammatory response
- Zollinger Ellison syndrome
- Triad of severe peptic ulcer disease + gastric acid hypersecretion + gastrinoma
- Characteristic finding is a fasting gastrin level of >1000pg/ml
- Associated with Multiple Endocrine Neoplasia Type 1 syndrome
How does peptic ulcer disease present?
- Retrosternal or epigastric pain
- Gastric is worse on eating, duodenal is worse 2-4 hours after eating or even alleviated by eating
- Nausea, bloating, post-prandial discomfort, early satiety
How would you investigate and manage peptic ulcer disease?
Investigations
- Nice says to do an urgent ogd for people with…
- New onset dysphagia
- >55 years old with weight loss and upper abdo pain/reflux/dyspepsia
- New dyspepsia not responding to ppi
- Ogd usually for older pts or red flag symptoms.
- Biopsy any peptic ulceration for histology and rapid urease test
- Most young low risk pts just need Non invasive h pylori testing
- Carbon 13 urea breath test
- Serum antibodies to h pylori
- Stool antigen test
Management
- Conservative
- Smoking cessation, weight loss, reduce alcohol
- Stop nsaids
- Start on PPI for 4-8 weeks then reassess
- Triple therapy for hpylori +ve (PPI + oral amoxi + clarithro OR metronidazole for 7 days)
- Surgery for Emergencies like perf or severe relapsing disease = partial gastrectomy or selective vagotomy