Why do my bowels not work?
For those that suffer constipation or painful diarrhoea due to faecal loading treatment needs to focus on three key elements.
Unless you address them all you will not have success 1/ a rectum that senses the faeces and provides
The urge to defecate, teemed with a correct defecatory technique and adequate pelvic floor function.
Most of my pts have dyssynergia defecation. When the patient tries to push the faeces out, instead of relaxing the EAS
(external anal sphincter) they either fail to relax it or actively contract the sphincter.
This leads to a feeling of incomplete emptying and a rectum that contains faeces after defecation (the rectum is supposed to be empty u til just prior to defecation)
Not only does dyssynergic defecation further slow down colonic transit it leads to rectal hyposensitivity. If left unchecked over years the pt will end up with a non functioning mega rectum that won’t ever work. Potentially needing a loop ileostomy.
Do NOT underestimate the importance of #Pelvicfloorphysiotherapy
2/ faeces that are of a soft enough consistency that the colon can move the faeces out.
In pts with POTS hypovolaemia leads to further dehydration and hardening of faeces. The faecal loading causes nausea and loss of appetite which reduces oral salt and water
This leads to less water in the colon and exacerbation of faecal loading, as well as driving the POTS which is causing the faecal loading in the first place
Gentle osmotic laxatives
3/ a colon that has enough motility. Post Covid GI dysfunction hEDs related
GI dysfunction leads to floppy bowels, with poor contractility. Further worsened by the connective tissue changes that lead to ptosis of the transverse colon and retention of faeces in the right colon.
Use a pro motility agent like Prucalopride.
If Prucalopride doesn’t work it usually means the faeces are still “too hard” to be moved by colonic peristalsis.
IV fluids a few litres a week for a few weeks will rehydrate the faeces from within, allowing the Prucalopride to start working.
SMAS
Superior mesenteric artery compression of the third part of the duodenum.
This usually cooccurs with Left renal vein compression by the SMA, because they both “sit” under and between the SMA and the aorta.
If MALS is thought to be then SMAS is thought to be a unicorn.
The irony is it is more common than MALS but…
Whilst the compression alone (ie not causing symptoms so can’t be called a VCS) is more common,
Symptomatic SMAS is less common than symptomatic MALS.
Diagnosis
This is where everything falls apart for those that have never seen an SMAS (most every gastro)
Most drs think it is the SMA being compressed like the CA is compressed in MALS) and fail to realise that symptoms are being caused by the SMA compressing D3.
MALS and SMAS
I have previously posted on vascular compression syndromes in trifecta pts.
I left the best to last.
Going thru medicine and gastro training we were never taught about these two syndromes.
Occasionally in a radiology meeting someone would
Through out MALS or SMAS as a cause of chronic unexplained pain and all the registrars and residents would quickly google it.
So what are these conditions?
In my previous post on VCS (vascular compression syndromes) I spoke about how they are almost universal
In POTS and hEDS pts?
This is true of both MALS and SMAS too.
The problem that arises then, is if they are so prevalent are they an incidental finding or the cause of symptoms?
My answer is, don’t do the test unless you are thinking that is the diagnosis, otherwise
I had an interesting letter back the other day from an immunologist looking after my pt. I had started her on Famotidine (H2 blocker) for her gut symptoms and as an antihistamine and Prucalopride (stimulates gut motility)
I view IBS as the gut manifestation of POTS and MCAS and treat all pts as having both diseases
Whilst it is always ideal to stagger introducing new meds in MCAS pts as inc risk of drug reactions and want to know which drug it is, the pt started both together.
The pt improved almost back to normal within a few weeks and the immunologist was surprised.
They were ix possibility of MCAS.
A comment they made for me thinking about the diagnostic criteria for MCAS, specifically “responds to mast cells directed treatment”
1 perforation
1 splenic rupture req splenectomy
Since cold snare polypectomy for large polyps and the use of clips my post polypectomy admission rate dropped from 1 every three years to 0 in last 3 years.
0 sepsis
Capsule endoscopy is designed to look at the small bowel not the large bowel.
CT colonoscopy is incredibly painful if I have IBS and if u find a polyp u then have to have a colonoscopy. Plus it misses the right sided sessile serrated adenomas which are more
Vascular Compression Syndromes (VCS) in POTS patients
In my experience, VCS are present in ALL patients with POTS, and are usually multiple. For the purposes of this thread this also applies to hEDS and trifecta patients as well.
So what is a VCS? A 🧵
A VCS is when a vascular structure (artery or vein) is either 1/ Being compressed by an adjacent structure or 2/ Is compressing an adj structure leading to the generation of symptoms
If the compression is asymptomatic we call it Vascular Compression Anatomy
The trouble with the definition of symptoms is "who gets to decide if the VC is sympt/asymptomatic?
Most VCS come to the attention of vascular surgeons, who r familiar with the typical presentations of VCS.
Most vascular surgeons are not familiar with POTS.
Another commone medication mistake in POTS
If I am using Ivabradine (or if on beta blockers, - I never use beta blockers) these drugs are usu given twice a day.
But what does twice a day mean to you and the pt, and why is twice a day diff for POTS pt?
HR control is a symptomatic treatment, if you standing and walking around the house HR is under 100 you may not need the second dose,
Particularly as POTS is worse in the morning. SO by the afternoon, your HR may be better and you may not need the second dose.
I tell my patients the second dose is optional depending upon how they feel, and as their POTS improves, they may be able to do away with the second dose
TIMING OF THE SECOND DOSE
Most pts will take the second dose 12 hours after the first dose, bd right? or in the evening
WRONG