Complications of Bariatric Surgery

Avoid "blind placement" of NG tubes
Avoid NSAIDs, ASA, plavix, steroids
Remember thiamine deficiency
Avoid overload of oral fluids

Consider compartment syndrome
Negative CT doesn't rule out a leak

Dysphagia - band slipage or gastric ischaemia
GI bleed - needs an endoscopy. May be from the anastamosis, gastric remnant. Consider octreotide.
Obstruction - may be a stricture, internal hernia. Bloating, hiccups, nausea, vomiting and abdo pain. Look on the AXR for an air fliud level in the gastric pouch. May be exacerbated by post op oedema.
Chest pain - may be PE, MI, pouch problem or anastomotic leak
Abdominal pain - subacute obstruction, anastomotic leak
Reflux - band slip, gastrojejunal stenosis.  May have more nausea and vomiting than non surgery.
Vomiting is not normal and needs a work up-  may be due to a band slip or stomal ulcers (less common. 2-4 months after surgery. Epigastric and retrosternal pain, dyspepsia, nausea and vomiting or an upper GI bleed.)
Gallstones ARE common after a roux-en-y
Remember thiamine and wenicke's, dehydration, and infection

Dumping Syndrome - for 12-18 months after the surgery. The small gastric pouch leads to rapid emptying of gastric contents into the small bowel, especially in carbohydrates. Treatment is to correct the hypotension, tachycardia, electrolyte disturbances and educate the patient to eat small, frequent, slow meals.


Roux-en-Y gastric bypass
Causes PE and anastomic leak are most common - most common in first week post op but can be a month after surgery. Symptoms may be subtle - tachycardia, dyspnoea, restlessness or mental state changes. The abdominal examination is often of limited value with no peritoneal signs.

Early post op complications include wound infection, dehiscence, acute GI obstruction, stomal stenosis, stomal/marginal ulcers, upper GI bleeding and dumping syndrome.

Stomach size shrinks and you get less gastric acid production

Band Gastroplasty
Lots of different options - less invasive option. Band is placed around the proximal stomach creating a restrictive pouch. The band is secured with sutures to prevent slipage, and can be adjusted

http://emergencymedicineireland.com/2015/10/tasty-morsels-of-em-058-bariatric-surgery-and-its-complications/
https://litfl.com/problems-after-bariatric-surgery/
https://www.bmj.com/content/352/bmj.i945

Back Examination

We do back pain examination every day, but it is worth remembering how to do it properly.

- Introduction, Consent, Handwashing, Chaparone. Exposure from the waist up

- Inspection
Inspection from the back and side for:
Cervical lordosis, thoracic kyphosis and lumbar lordosis (lost with age, ank spond, acute disc prolapse).
Cafe au lait spots (neurofibromatosis), hairy patch (spinal dysraphism)
Muscle wasting
Scars

- Palpation
For temperature
  Palpate each spinous process
  Palpate sacroiliac joints
  Palpate paraspinal muscles
Percuss with a fist or tendon hammer (infection, fracture or tumour)

- Move
Lumbar: Lumbar flexion, extension and lateral flexion.
   run hands down side (lateral flexion)
   touch their toes with knees straight (flexion)
   lean backwards with knes straight (extension) - no extension in facet disease.
  Can do a modified Schobers Test - place index and middle fingers 5 centimeters apart and noting how close and far apart they move on the movements.

C-Spine 
Lateral flexion: place your ear on your shoulder;
rotation: look over your shoulder;
flexion: put your chin on your chest;
extension: put your head back to look at the ceiling.

Thoracic 
Fix pelvis and turn

- Special Tests
Straight leg raise - to look for sciatica
Sciatic nerve test - do SLR. When pain brought on, dorsiflex the foot = positive = sciatic!
Bowstring test - SLR. Then lower. Apply popliteal compression = symptoms.

Femoral nerve stretch test - lie prone, passively flex knee - severe = positive.
Tiptoe test - tests S1
Duck walk (on heels) - for L4 power

Neurological examination

References

http://www.osceskills.com/e-learning/subjects/spine-examination/

Back Pain

HAP2 on back pain and CAP3 include more than you think they might. Life threatening and abdominal causes of back pain are covered elsewhere. Here are some links on general back pain, cauda equina, spinal cord compression and osteoporosis.

Enlighten Me
Back pain module  
Back pain in a young person -
I've gone numb down there
Paediatric Back Pain
Not what I was expecting

BMJ Learning
Metastatic Spinal Cord Compression
Back Examination
Cord Compression
Osteoporosis

Doctors.net
Back Pain
Osteoporosis

Back Pain

Low back pain: pain between the lower costal margin and gluteal folds, which may be accompanied by leg pain.

Back pain is common and has a huge socio-economic cost, and can be life threatening for the patient. We should not use the bio-medical model of injury (emphasis on looking for pathological lesion that causes back pain) as this is likely to cause over-investigation.

5% of people have a diagnosable condition
<1% have a serious medical condition
Most resolves in 6-8 weeks

History and examination should cover red flags, yellow flags, and nerve root problems.

Red Flags: for possible serious spinal pathology when assessing back pain:

• non-mechanical pain
• past history carcinoma, steroids, HIV
• generally unwell
• unexplained weight loss
• widespread neurological symptom or signs
• structural deformity
• thoracic pain
• Age <20 years or >55 years has also been considered a red flag, but it should be borne in mind that non-specific back pain is not uncommon in these age groups. Significant trauma may raise the possibility of vertebral fracture.

Yellow Flags:  risk factors for developing and or maintaining long-term pain and disability
- Belief that pain and activity is harmful
- Belief that pain will persist
- Sickness, avoidant and excessive safety behaviours (like extended rest, guarded movements)
- Low or negative moods, anger, distress, social withdrawal
- Treatment that does not fit with best practice
- Claims and compensation for pain-related disability
- Problems with work, sickness absence, low job satisfaction
- Overprotective family or lack of support
- Placing responsibility on others to get them better (external locus of control)

Indicators for nerve root problems:
- Unilateral leg pain and low back pain
- Radiates to foot or toes
- Numbness or paraesthesia in same distribution
- Straight leg raising test induces more leg pain
- Localised neurology (limited to one nerve root)

Examination
Sacroiliac joints: Lie supine and apply firm downward pressure over both sides of the pelvis

Straight leg raise test: suggestive of nerve root pain.
    Ask the patient to lie flat on their back
    Raise the patient's leg and ask them to tell you when they feel pain in thigh, buttock, and calf
        The leg must be completely straight
        The test is positive if pain occurs with the leg at an angle of less than 70°
    It is normal to experience pain with the leg at an angle of 80-90° with the bed.

Sciatic stretch test:
    Dorsiflex the foot with the leg still raised
        The test is positive if the patient experiences further discomfort in the thigh, buttock, and calf
    The pain should be relieved by bending the knee.

You should repeat both tests on the unaffected leg. You should suspect a prolapsed intervertebral disc in patients who experience pain in the affected leg when you raise the unaffected leg. You should make an urgent referral in these patients because they are at risk of developing cauda equina syndrome.

The leg must be raised 30° above the bed. Below this angle the sciatic nerve is not stretched. You should consider an alternative diagnosis such as arthritis in patients who experience pain with the leg below a 30° angle.


Femoral Stretch Test:

Imaging
Imaging is unlikely to be helpful, even MRISs. In asymptomatic people, MRIs show:
- Bulging discs in 20% to 79%
- Herniated discs in 9% to 76%
- Degenerative discs in 46% to 91%.

Sciatica
50% of patients with sciatica will recover from the acute attack within 6 weeks. Over a third of back pain cases will have accompanying leg pain, true nerve root pain has a prevalence of around 4%, and "surgically important" root pain is as low as 2%.

Cauda Equina

Spinal Cord Compression

3-5% of patients with cancer develop bone metastasis. If they have a high risk cancer this rises to 20%. Mets may occur years after the primary cancer diagnosis.
Only about 1/2 of patients with SCC will have a high risk cancer. 20-25% have no existing cancer diagnosis.
17% of patients have lesions at two or more levels so the entire scan should be MRId. Spinal cord compression often occurs in the last year of life.

Symptoms:
    Back pain (95% of patients), radiating (in 37%) or localised (15%).
    Spinal pain aggravated by straining (for example, when coughing)
    Nocturnal spinal pain which interferes with sleep.

    

    Limb weakness (87% of patients)

    Paraplegia (18%) 

    Painless urinary retention

Signs:

Patients who have primarily compression of the posterior cord may lose proprioception, and so have difficulty walking, but may have normal muscle power on assessment.
Symptoms and/or signs of spinal cord compression may become more obvious if you load the patient's spine, eg by getting them to carefully stand and walk - providing they do not have significant movement related spinal pain

Imaging:

Plain x-rays need up to 50% bone loss before lesions become visible.
CT  may show supplemental information

MRI is the main imaging modality

Treatment:
Radiotherapy will help a tumour
Nurse patients flat wit neutral spinal alignment, log roll, and use a bed pan.
16mg dexamethasone

Osteoporosis

Think about prophylaxis before the patient gets a fracture. The FRAX score is very useful. 

Alendronate is the first line treatment. Alendronate can cause dyspepsia, but we shouldn't start at PPI because it’s not an acid related dyspepsia. There is  evidence to suggest that PPIs and H2RAs actually increase the risk of fracture.

Aortic Disection

Doctors.net 
EnlightenMe
Potential use of d-dimers
Hypertensive Emergency
Walking Problems
Chest X-ray
CEMPaedia
Collapse and Shock
Clot or Bleeding
 
BMJ Learning
Learning Module
Article

FOAM
http://emcrit.org/podcasts/aortic-dissection/
http://lifeinthefastlane.com/education/ccc/acute-aortic-dissection/
http://lifeinthefastlane.com/2010/03/cardiovascular-curveball-008/
http://lifeinthefastlane.com/2010/09/die-like-a-king/
http://lifeinthefastlane.com/2008/11/aortic-dissection-lecture-notes/
http://flippedemclassroom.wordpress.com/2013/06/07/aortic-dissection/
http://academiclifeinem.com/paucis-verbis-international-registry-on-aortic-dissection-irad/

Pathophysiology
Aortic disection is caused by a disruption of the media layer of the aorta. For this to start, this needs a tear of intima with the formation of a false lumen between layers. An important variation of ATAD is an acute intramural haematoma - bleeding within the wall without an intimal defect. The treatment is the same.

There are three possibilities as to how the blood gets into the media:
-    Atherosclerotic ulcer leading to intimal tear
-    Disruption of vasa vasorum causing intramural haematoma
-    De novo intimal tear

Most tears occur in the ascending aorta due to greater pressure on the aortic wall. Once the dissection process occurs blood tracks through the media to varying degrees and may dissect down from the aortic root to the bifurcation of the common iliac arteries in a matter of seconds.

                  Location of primary aortic tear     Incidence
                  Ascending aorta                           70%
                  Descending thoracic aorta            15-20%
                  Arch of the aorta                          10%
                  Abdominal aorta                           <5%




Risk Factors
Thrombus - 2/3 of patients
Embolism - 1/3 of patients

White (79%)
Men (68%)
over 40



Inherited disease (especially younger patients < 40 yrs)
 - Marfan’s syndrome (fibrillin gene mutations)
 - Ehlers-Danlos syndrome type IV (collagen defects)
 - Turner syndrome
 - annulo- aortic ectasia
 - familial aortic dissection.

    
Aortic wall stress 
- Hypertension (72%)
- Previous cardiovascular surgery
- Bicuspid or unicommisural aortic valve
- Aortic coarctation
- Iatrogenic
- Infection (syphilis)
- Arteritis such as Takayasu’s or giant cell, aortic dilatation / aneurysm, wall thinning
- ‘crack’ cocaine (abrupt catecholamine-induced hypertension).

Reduced resistance aortic wall 
- Increasing age
- pregnancy (debatable).

Clinical Symptoms

The clinical symptoms vary depending on which branch vessel is occluded:
Coronary vessel(s)                    ST elevation myocardial infarction
Common carotid(s)                   any type of stroke
Subclavian(s)                            an acutely ischaemic upper limb
Coeliac/mesenteric vessel(s)      ischaemic bowel
Renal vessel(s)                          frank haematuria
Spinal artery(ies)                       sudden onset painless paraplegia

Ascending aorta:                       haemopericardium (syncope and /or sudden death)
                                                right haemothorax (invariably sudden death)
Arch of aorta:                           mediastinal haematoma
                                                interatrial septal haematoma (cardiac conduction defects)
                                                compression of pulmonary trunk/ artery
Descending aorta:                     left haemothorax (sudden death)
                                                rarely into oesophagus (profuse haematemesis)
Abdominal aorta:                      retroperitoneal haemorrhage (back pain with shock)
                                                rarely intraperitoneal haemorrhage (shock and acute abdomen)
Aortic root:                              aortic regurgitation can occur when the dissection process extends into or around the aortic valvular support. The aortic root can dilate so much that the aortic leaflets cannot fully appose during diastole, allowing regurgitation of blood. 

Pain
Pain is the most common symptom. 
The pain is said to be severe or ‘worst ever’ (90%), abrupt (90%), sharp (64%) or tearing (50%) retrosternal or interscapular pain (50%), migrating (16%), down the back (46%), maximal at onset (not crescendo build up, as in an AMI).

The pain in aortic dissection occurs in the anterior chest 70-80% of the time in patients with a type A dissection and back pain occurs only in 50% of all patients. Abdominal pain was found to be the third commonest site of initial pain and other sites described were the throat, neck and extremities.

Patients may also describe the classic migration of pain from the chest, back or abdomen to one or more limbs or to the neck and this is thought to be due to peripheral extension of the dissection from the primary intimal tear.

In 5-15% of patients however, no pain occurs at all. This is typically the case in those patients presenting with syncope, stroke, congestive cardiac failure or the elderly. 

Cardiac Signs
- Aortic incompetence (32%)
- cardiac tamponade, 
- myocardial ischaemia (although only 2-5% of ECGs mimick AMI)
-  BP differences >20 mmHg in arms
- missing pulse (15%).
        
Other Signs
- Pleural rub or effusion, haemothorax
- Altered consciousness
- syncope (13 %), 
- hemiplegia (5%)
- paraplegia.
 - abdominal pain (43% descending, 22% ascending)
- intestinal ischaemia 
- oliguria
 
Diagnosis
Transthoracic Echocardiography -  78.3% sensitivity and 83.0% specificity for diagnosing proximal dissection. Cannot accurately visualise the descending aorta in most patients. Can diagnose aortic incompetence. 
May identify a free intimal flap within the aortic lumen - sensitivity is approximately 80% for type A dissections but only 50% for type B. 

CT - 83-100% sensitive
  Will reveal pericardial fluid which will suggest dissection diagnosis in the right clinical context. 
 
ECG - normal in 30% of cases
   STEMI patterns in 3% (Changes consistently with AMI do not rule out dissection)
   15% acute ischaemic changes
   41% had non-specific ST segment and T wave changes

Chest X-ray - normal in 12% of cases
   Mediastinal widening in 60% of cases 
   Abnormal aortic contour 50% of cases
   Soft tissue shadow behind a calcified aortic annulus (15%)
   Globular heart (haemopericardium) 
   Pleural effusion (haemothorax)  


 
Bloods - D-dimer has a sensitivity of below 95%

Treatment
The most important step in treatment is diagnosis - 40% cases are initially misdiagnosed. Mortality increases every hour from onset of disease.


Even if there are signs of tamponade, do not perform pericardiocentesis. 

There are two main types of disection: 
     Stanford A: De Bakey 1 and II: Proximal
     Stanford B: Proximal
     Stanford B: DeBakey IIIa and IIIb: Distal
     Stanford A dissections normally have surgical treatment, and type B has medical management.  
 
 
Medical Management
Analgesia
Blood Pressure Control:
 - Control blood pressure with labetalol (a mixed alpha and beta blockers)
  - Causes vasodilatation and reduces cardiac contractility
 - Doesn't cause reflex tachycardia that is seen with other vasodilators. 
Best to use a mixture of beta blockers and vasodilators - so metoprolol and GTN

  
Ten year survival rates of patients who are discharged from hospital range from 30% to 60%