I’ve finished with my haematology firm. Overall, it was one of my favourite firms purely because the consultant actually knew our names and got to know us, so when it came to signing us off, he wrote a rave review rather than the generic ‘has a good patient manner’. The only downside was that because it is a super specialist firm, there are no F1s and as a medical student, the F1s are your favourite people. They are not that much older than you, usually non-intimidating, know what you need to know for your level and can point out the good patients to see. Today I went to AAU (acute assessment unit) and clerked a treasure chest patient (totally just made up that phrase, but I like it) with loads of signs. One of the F1s pointed him out because F1s are wonderful people.
And here is my would be verbal presentation:
“Today I performed a cardiovascular examination on an 86 year-old gentlemen presenting with two episodes of collapse. On examination he appeared comfortable at rest but reported left shoulder pain. There was no paraphernalia around the bedside suggestive of cardiovascular disease. On examination of his hands, there was a ‘pill-rolling’ tremor of his right hand, suggestive of Parkinson’s disease. Capillary refill time was less than 2 seconds and radial pulse was 64 bpm. There were no further peripheral stigmata of cardiovascular disease on the hands or face. Carotid pulse was normal in volume and character. On closer inspection of the chest, there was a midline sternotomy scar (from CABG) and a pacemaker below the left clavicle. On palpation of the chest, I could not feel the apex beat (because I am rubbish at feeling the apex beat) and there were no palpable heaves or thrills. On auscultation, heart sounds 1 and 2 were present but were muffled by a very loud ejection systolic murmur that was loudest in the aortic region and did not radiate to the carotids. Lung bases were clear and there was no sacral or bipedal oedema.”
Signs make me happy 🙂
And here is a totally unrelated change of topic:
Definition: obstruction of the normal movement of bowel contents. Obstruction can be in the small or large bowel. There may be an ileus- functional obstruction- or mechanical obstruction. Mechanical obstruction can be simple, with one obstructing point and no vascular compromise; closed loop, with two obstructing points; or strangulated, with compromised blood supply. Obstruction can also be partial or complete.
Aetiology/ risk factors:
Small bowel- adhesions (fibrous bands in the abdomen that occur after surgery, sticking everything together and annoying the hell out of surgeons when they need to go back into the abdomen and pry all the adhesions apart to get to the bowel), hernias
Large bowel- colon cancer, constipation, diverticular stricture, volvulus
VOLVULUS = sigmoid (65%)/ caecal (30%) volvulus is when the bowel twists on its mesentery, which can produce severe, rapid, strangulated obstruction. This tends to occur in the elderly, constipated and comorbid patient.
Associations: anatomical factors, such as long sigmoid mesentery, mobile caecum, chronic constipation and debility, age, very high residue diet, adhesions, Chaga’s disease of the colon.
Causes ∼5-10% of large bowel obstruction.
A 360º twist can compress and occlude the veins to the bowel, leading to circulatory impairment, and if not relieved, gangrene and perforation.
There may be a history of previous episodes with spontaneous resolution.
Rare– Crohn’s stricture, gallstone ileus (gallstone gets stuck in small bowel), intussusception (part of the intestine folds into another section of intestine), TB, foreign body
–Ileus– adynamic bowel due to absence of normal peristaltic contractions.
Contributing factors: abdominal surgery, pancreatitis, spinal injury, hypokalaemia, hyponatraemia, uraemia, peritoneal sepsis and drugs e.g. tricyclic anti-depressants.
–Pseudo-obstruction- like mechanical GI obstruction but no cause for obstruction found. Features similar to mechanical obstruction.
Predisposing factors: post-partum, pelvic surgery, trauma, cardiorespiratory disorders.
Epidemiology: common, more so in elderly due to increased incidence of adhesions, hernias, and malignancy.
–vomiting + colicky abdominal pain + constipation + distension
greenish bile-stained vomit in early small bowel obstruction and ‘faeculent’ vomiting (fermentation of intestinal contents) later in lower small bowel, and large bowel obstruction
colic occurs early and may be absent in long-standing obstruction
constipation need not be absolute (no faeces or flatus) if obstruction is high, but in distal obstruction (e.g. colonic volvulus), nothing is passed
-In small bowel obstruction, vomiting occurs earlier, distension is less, and pain is higher in the abdomen (centre).
-In large bowel obstruction, pain is more constant and lower in the abdomen.
-In ileus, pain is not a feature.
-Chronic pseudo-obstruction presents with weight loss from malabsorption.
–Strangulation– pain is sharper, more constant and localised.
-abdominal distension- more marked as obstruction progresses
-visible peristalsis may be seen
-‘tinkling’ bowel sounds in mechanical obstruction. Bowel sounds may be absent if peritonitis has developed.
-in ileus- bowel sounds are absent
–Closed loop obstruction: tenderness over a distended caecum = obstruction with competent ileocaecal valve, forming a loop of grossly distended bowel, at risk of perforation as the bowel is thinnest and widest at the caecum (> 12cm = urgent decompression)
–Strangulation: peritonism- abdominal guarding, rebound tenderness- fever
(Peritonism occurs as a lack of blood supply impairs the mucosal barrier function causing bacterial transudation into the peritoneal cavity.)
Bloods- FBC (↑WCC in strangulation),
U&ES (dehydration, electrolyte abnormalities due to vomiting), Amylase
ABG- lactic acidosis may suggest bowel ischaemia and impending perforation
Microcytic anaemia- suggests large bowel malignancy
Small bowel obstruction- central gas shadows with valvulae conniventes that completely cross the lumen (central ladder pattern of distended loops) and no gas in the large bowel.
This is small bowel because it is central and the lines (valvulae conniventes) cross the whole width.
Large bowel obstruction- distended bowel lies more peripherally. Shows peripheral gas shadows proximal to the blockage, but not in the rectum (unless you’ve done a PR exam). Large bowel haustra do not cross all the lumen’s width.
Dilated bowel is in the peripheries and does not have lines going all the way across, so it’s large bowel.
Volvulus- Sigmoid volvulus has a characteristic AXR appearance: ‘inverted U’ loop of bowel that looks a bit like a coffee bean. In caecal volvulus, the concavity d the coffee bean points towards the right lower quadrant, and in sigmoid, to the left.
May be associated with proximally dilated loops of bowel and distal collapse.
This is sigmoid volvulus- see the massive coffee bean?
Erect CXR- gas under diaphragm in bowel perforation
CT- if clinical and x-ray findings inconclusive. Finds cause and level of obstruction. May show dilated, fluid-filled bowel and a transition zone at the site of obstruction.
In volvulus, CT identifies rotation of the mesentery and bowel as well as signs of ischemia.
Colonoscopy- in some cases, may be used to investigate causes of mechanical large bowel obstruction e.g. tumour, but there is a danger of causing perforation in the acute setting.
Oral Gastrografin– can help identify partial small bowel obstruction (= see how long it takes for this contrast to reach the colon) and may also have mild therapeutic action against mechanical obstruction.
Water-soluble contrast enema- can demonstrate the site of large bowel obstruction
In sigmoid volvulus, there is a ‘bird’s beak’ or ‘ace of spades’ deformity with spiral narrowing of the distal bowel at the site.
Bird’s beak at obstruction site
-Strangulation and large bowel obstruction require surgery
-Ileus and incomplete small bowel obstruction can be managed conservatively, at least to start off
-‘Drip and suck’- IV fluids (rehydrate, correct electrolyte imbalances) and NG tube (aspirate GI contents out = decompression of upper GIT) + NBM
-Catheterise to monitor fluid status
-ABx if signs of ischaemia or sepsis
-Conservative measures may settle an acute obstruction; however, if not resolving or signs of complications, an early operation can be planned.
Strangulation & closed loop obstruction need emergency surgery.
Stents may be used for obstructing large bowel malignancies, as a palliative measure or as a bridge to surgery in acute obstruction.
Surgery may involve adhesiolysis or bowel resection +/- stoma +/- primary anastomosis +/- Hartmann’s.
Small bowel obstruction secondary to adhesions rarely needs surgery.
Volvulus– sigmoid volvulus is often managed by sigmoidoscopy and insertion of a flatus (rectal) tube. Sigmoid colectomy (cut out the sigmoid) is sometimes required.
If signs of peritonitis, bowel ischaemia or failure of conservative measures- laparotomy, untwisting, resection of dilated, gangrenous or ischaemic colon, with either a primary anastomosis and/or stoma.
Caecal volvulus- ileocaecal resection, right hemicolectomy, or caecopexy (fix caecum to abdominal wall) is performed.
Pseudo-obstruction- neostigmine (cholinesterase inhibitor) or colonoscopic decompression sometimes useful in acute colonic pseudo-obstruction (Ogilvie’s syndrome)
-Bowel perforation- especially in closed loop obstruction i.e. obstruction at two points, such as a sigmoid volvulus with distended proximal colon and a competent ileocaecal valve. Even with simple obstruction, with increased distension, the intestinal wall blood supply becomes impaired and mucosal ulceration and bowel perforation may occur.
-Strangulation, mesenteric ischaemia, gangrene of ischaemic bowel wall
Prognosis: variable. Depends on the general state of patients and the prevalence of complications.
-Though management is often effective, recurrence of volvulus is common. Overall mortality of sigmoid volvulus can be as high as 20%.