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YR3 Gastro > Miscellaneous GI conditions > Flashcards

Miscellaneous GI conditions Flashcards

obstructions, hernias, peritonitis

1
Q

Define amyloidosis and amyloid deposit

A

Amyloid deposit:

Any histological tissue specimen that binds Congo Red + demonstrates green befringence under polarised light

Amyloidosis:

Deposits of amyloid, either localised in tissue or as part of a systemic process, leading to organ dysfunction

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2
Q

Explain the pathophysiology of amyloidosis

A

Misfolding of immunoglobulin light chains into amyloid configuration

Go from being soluble → insoluble

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5
Q

Describe the types of amyloidosis and the organs they affect

A
  • Type AA - serum amyloid A protein
    • Also known as secondary amyloidosis
    • Affects kidneys, liver and spleen
  • Type AL - monoclonal immunoglobulin light chains
    • Also known as primary amyloidosis
    • Affects kidneys, heart, nerves, gut, vascular
  • Type ATTR (familial amyloid polyneuropathy) - genetic-variant transthyretin
    • Also known as familial amyloidosis
    • Usually causes a sensory or autonomic neuropathy +/- renal or cardiac involvement
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6
Q

Recognise the presenting symptoms and signs of amyloidosis

A
  • Renal - proteinuria, nephrotic syndrome, renal failure
  • Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina
  • GI - macroglossia (characteristic of AL), hepatosplenomegaly, gut dysmotility, malabsorption, bleeding
  • Neurological - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome
  • Skin - waxy skin and easy bruising, purpura around the eyes (characteristic of AL), plaques and nodules
  • Joints - painful asymmetrical large joints, enlargement of anterior shoulder
  • Haematological - bleeding tendenc
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7
Q

Define appendicitis

A

acute inflammation of the vermiform appendix

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8
Q

Summarise the epidemiology of appendicitis

A
  • Most common surgical emergency
  • Commonest early teens- late 40s
  • Overall lifetime risk of developing acute appendicitis:
    • 8.6% M
    • 6.7% F
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9
Q

Explain the pathophysiology of appendicitis

A

Most commonly caused by obstruction of the lumen of the appendix by:

  • faecolith (hard mass of faecal matter)
  • normal stool
  • lymphoid hyperplasia of Peyer’s patches
  • Fibrous strictures from previous inflammation

Distal to the obstruciton, the appendix fills with mucus → distension + bacterial overgrowth

Inflammation irritates the parietal peritoneum leading to RLQ pain

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10
Q

What are the bacteria most commonly present in appendicitis?

A

Bacteroides fragilis

E. Coli

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11
Q

What are the risk factors for appendicitis?

A
  • Frequent use of antibiotics and improved hygienic conditions
    • lead to decreased exposure and/or imbalance of gastrointestinal microbial flora
  • Low dietry fibre
  • Smoking
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12
Q

Explain the shifting in pain sensation in appendicits

A

Pain originates in the midline and moves to the right iliac fossa

  • Initial pain is due to inflammation of the visceral peritoneum and appendix itself (a midgut organ, lesser splanchnic)
    • Visceral pain tends to be poorly localised and the pain is referred to the midline.
  • As the inflammation spreads to the parietal peritoneum, which is somatosensory, it is localised at the RIF
  • This shift in pain location usually occurs in <24 hours.
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13
Q

What are the presenting symptoms of appendicitis?

A
  • Periumbilical pain moving to the right iliac fossa
  • Anorexia
    • if PT wants to eat, unlikely appendicitis
  • N+V
    • ​due to pain, obstruction
  • Low grade pyrexia
  • Quiet bowel sounds- in perforation
  • Localised peritonitis with guarding
    • in perforation, pregnancy
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14
Q

What are the classic signs of appendicitis on physical examination?

A

In perforation

  • Quiet bowel sounds
  • Localised peritonitis with guarding + rebound tenderness

signs:

  • Psoas sign
    • pain on extension of the hip
    • due to inflammation of psoas by appendix
  • Rovsing’s sign
    • palpation of the LIF causes more pain on the RIF than LIF
  • Obturator sign
    • pain on flexion and internal rotation of hip
    • due to inflammation of obturator by appendix
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15
Q

What investigations would you do for appendicitis?

A
  • FBC
    • Mild leukocytosis with neutrophilia
  • CRP
    • elevated
  • abdominal ultrasound
    • detect gynae issues/other causes of pain
    • if normal appendix viewed fully, can rule out appendicitis
  • contrast-enhanced abdominal CT
    • high diagnostic accuracy but may cause fatal delay – usually go straight to surgery for diagnostic laparoscopy +/- appendicectomy
  • urinalysis- exclude UTI
  • pregnancy test- exclude ectopic
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16
Q

How is appendicitis managed?

A
  • Prompt appendicectomy
    • ​laparoscopy - diagnostic and therapeutic advantages
  • Antibiotics:
    • Cefuroxime
    • Metronidazole
  • Supportive treatment
    • ​analgesia- morphine sulfate, IV paracetamol
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17
Q

Identify the possible complications of appendicitis

A
  • Perforation
  • Appendix mass
    • Occurs when the inflamed appendix becomes covered with omentum
  • Appendix abscess
    • May occur if appendix mass fails to resolve
    • Treatment involves drainage and antibiotics
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18
Q

Define hernia

A

protrusion of a viscus or part of a viscus through a defect of the wall of its containing cavity into an abnormal position.

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19
Q

How do you differentiate between inguinal and femoral hernias?

A

FEMORAL = inferolateral to the pubic tubercle, medial to the femoral artery

INGUINAL = superomedial to the pubic tubercle

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20
Q

What, in general, causes hernias? give some exampels

A

Increase in intra-abdominal pressure

i.e. due to:

  • chronic cough
  • smoking causing cough
  • constipation
  • pregnancy
  • weight-lifting
  • weakened abdominal muscles.
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21
Q

In the context of hernias, define:

  • incarcerated
  • strangulated
  • irreduceable
  • obstructed
A
  • incarcerated- contents of the hernia are stuck by adhesions
  • strangulated- if ischaemia occurs
  • irreduceable - cannot be pushed back into right position
  • obstructed- hernia is causing an obstruction
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22
Q

Describe the location and contents of the inguinal ligament

A

Runs between the pubic tubercle and the ASIS

within the ligament is the inguinal canal, containing:

  • spermatic cord (M)
  • round ligament (F)
  • ilioinguinal nerve (both)
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23
Q

Where is the entry and exit points of the uinguinal canal?

A

enters at the deep inguinal ring

  • this is halfway between the ASIS and pubic tubercle - midpoint of tubercle

emerges at the superficial ring

  • superomedial to pubic tubercle
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24
Q

Define inguinal hernia, state the 2 classifications

A

Protrusion of abdmonial or pelvic contents out of the external inguinal ring, causing a visible or easily palpable bulge.

direct:

  • contents travel directly through a weakness in the posterior wall of inguinal canal, medial to deep ring

indirect:

  • protrusion of the hernia sack through a dilated deep inguinal ring
  • follows path of inguinal canal
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25
Q

Explain the risk factors of inguinal hernias

A
  • male sex (27% lifetime risk)
  • older age
  • smoking- weakness in connective tissue
  • family history
  • prematurity
  • AAA
  • previous abdominal surgery
  • obesity
  • chronic cough- eg by chronic bronchitis, emphysema
  • pregnancy
  • ascites
  • connective tissue disorders- Marfan, Ehlders Danlos
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26
Q

Summarise the epidemiology of inguinal hernias

A

COMMON

Peak age in adults: 55-85 yrs

9 x more common in MALES

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27
Q

Recognise the presenting symptoms of inguinal hernias

A

Inguinal hernias have 4 basic presentations:

  • Asymptomatic groin swelling or bulge
  • Symptomatic groin swelling or bulge
  • Inguinoscrotal swelling
  • Acute abdomen (rare).
    • ​If the hernia is obstructed or strangulated, the patient may present with severe abdominal pain, nausea and vomiting.

Pain associated with a hernia is felt only when the hernia is bulging, unlike pain from a groin injury

Bulge may be intermittent or disappear when lying flat

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28
Q

Recognise the signs of inguinal hernias on physical examination

A

ACUTE ABDO:

  • May be irreducible, tender, with absent bowel sounds.

GROIN SWELLING:

  • Assymmetry in the groin region
  • Bulge detected by palpation with thumb over internal and external ring areas
  • Valsalva manoeuvre/cough- palpate during manouvre
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29
Q

How do you discerne between direct and indirect inguinal hernias

A

Reduce the hernia and occlude the deep internal ring with two fingers.

Ask patient to cough/stand. If hernia is restrained, it is indirect. If not, it is direct

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30
Q

Identify appropriate investigations for inguinal hernias

A

Most inguinal hernias are diagnosed clinically by observation and palpation

Imaging may be useful when there is diagnostic uncertainty

  • USS/MRI- occult hernia
  • CT- in obese patients

If acute- full blood panel, ABG show lactic acidosis due to strangulation

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31
Q

How are inguinal hernias mangement

A

Watchful waiting is considered a safe strategy in adults with minimally symptomatic or asymptomatic hernia

Surgery - only if hernia becomes symptomatic

  • elective laparoscopic or open mesh repair
    • hernia is surgically reduced, mesh reinforces the damaged transversalis fascia
    • laparoscopic requires more skill
  • emergency repair of incarcerted/strangulated hernia
    • laparotomy with bowel resection if gangrenous
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32
Q

Identify possible complications of inguinal hernias

A
  • Incarceration
  • Strangulation
  • Bowel obstruction
  • Maydl’s hernia (image on the right - strangulated W-shaped loop of small bowel)
  • Richter’s hernia (strangulation of only part of the bowel circumference)
  • Complications of surgery
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33
Q

Summarise the prognosis for patients with inguinal hernias

A

Prognosis is excellent after surgical repair

Slowly enlarge if left alone

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34
Q

Define Femoral Hernia

A

Abdominal contents pass through weakness femoral canal, presenting as a mass in the upper medial thigh

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35
Q

What is the epidemiology of femoral hernias

A
  • Less common than inguinal but these are more likely to get incarcerated as they are situated in a tighter place.
  • More commen in women – especially slim, middle age-elderly
  • Account for 5% of abdominal hernias
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36
Q

Explain the risk factors of femoral hernias

A
  • Female
  • Increasing age
  • Pregnancy – higher incidence in multiparous compared to nulliparous
  • Increased intra-abdominal pressure e.g. heavy lifting, chronic constipation
37
Q

What are the presenting symptoms of femoral hernias?

A

Lump in groin, inferior to inguinal ligament

Usually asymptomatic at presentation

Around 30% present as an emergency due to obstruction or strangulation

38
Q

Define intestinal (mesenteric) ischaemia

A

Ischaemic bowel disease encompasses a heterogeneous group of disorders caused by acute or chronic processes

arising from occlusive or non-occlusive aetiologies, which result in decreased blood flow to the gastrointestinal tract.

Note: AF with abdominal pain should point towards mesenteric ischaemia

39
Q

What are the 3 main types of ischaemic bowel disease?

A
  1. acute mesenteric ischaemia
  2. chronic mesenteric ischaemia (mesenteric angina)
  3. chronic colonic ischaemia- ischaemic colitis
40
Q

Explain the aetiology/risk factors of mesenteric ishcaemia

A
  • Embolism- 50%
    • usually from LH thrombus or aortic plaque rupture
  • Thrombosis- 15-20%
    • progression from SMA atherosclerosis
    • atherosclerosis seen in chronic ischaemia
  • Vasculitis
    • from SLE, Rheumatoid arthritis
  • External compression
    • from tumour, median arucurate ligament compression
  • Venous thrombosis
    • SMV- due to portal hypertension, cirrhosis, hypercoagulable disorders
  • Hypoperfusion- 20%
    • hypotension, shock
    • HF, dialysis, surgery (AAA, colectomy) trauma
41
Q

Which areas of the bowel are most affected by hypoperfusion?

A

Washershed areas

Regions of the gut which recieve dual blood supply

They are protected from infarctions but affected worse in hypoperfusion as they are supplied from most distal branches of 2 arteries

42
Q

Define ischaemic colitis

A

Inflammation of the colon caused by decreased colonic blood supply.

Usually follows low flow state in inferior mesenteric artery.

Ischaemia leads to mucosal inflammation, oedema, necrosis and ulceration

43
Q

What are the risk factors for mesenteric ischaemia?

A

2 main causes:

1: low flow states leading to generalised colonic ischaemia

  • Hx of vasculitis
  • Shock
  • CHF
  • smoking- often associated with hypertension and PVD

2: emboli causing acute mesenteric ischaemia

  • recent cardiovascular surgery
  • hypercoagulable states (factor V Leiden, protein C deficiency)
  • AF/MI/endocarditis - throws clots which embolise
  • structural heart defects
44
Q

Summarise the epidemiology of intestinal ischaemia

A

Colonic ischaemia frequently occurs in older people with co-existing morbidities

  • colonic ischaemia is common in IBS, recent cardiovascular surgery, constipation
  • acute mesenteric ischaemia is common in MI, AF and atherosclerosis
45
Q

Recognise the presenting symptoms of intestinal ischaemia

A

Abdominal pain varies depending on location + extent of ischaemia

  • Acute mesenteric ischaemia:
    • acute severe abdominal pain + no abdominal signs + rapid hypovolaemia shock
    • Pain tends to be constant, central or around RIF
  • Chronic mesenteric ischaemia:
    • ​severe, colicky post-prandial abdominal pain (gut claudication)
    • +/- upper abdominal bruit
    • +/- PR bleeding
  • Chronic colonic ischaemia:
    • ​lower left-sided abdominal pain
    • +/- bloody diarrhoea
46
Q

State some general symptoms of intestinal ischaemia

A
  • Fever
  • Severe acute colicky abdominal pain
  • Vomiting
  • Nausea
  • Bloody diarrhoea
  • History of chronic mesenteric artery insufficiency
  • Gross weight loss
  • Post-prandial abdominal pain
  • History of heart or liver disease
47
Q

Recognise the signs of intestinal ischaemia on physical examination

A
  • Fever and tachycardia
  • Diffuse abdominal tenderness
  • Abdominal distension
  • Tender palpable mass (ischaemic bowel)
  • Bowel sounds may be absent
  • Disproportionate degree of cardiovascular collapse
  • Upper abdominal bruit
48
Q

Identify appropriate investigations for intestinal ischaemia

A

Diagnosis based on clinical suspicion or after laparotomy

  • AXR - thickening of small bowel folds and signs of obstruction, early on shows ‘gas less abdomen’
  • Bloods
    • ABG - lactic acidosis
    • FBC – low Hb due to plasma loss, high WCC
    • U&Es
    • LFTs
    • Clotting
    • Cross-match
  • Mesenteric Angiography
    • Only if stable
    • CT/MR angiography are replacing traditional angiography
  • For ischaemic colitis, colonoscopy and biopsy is gold-standard. Barium enema shows characteristic ‘thumb printing’ of submucosal swelling.
49
Q

Define and classify intestinal obstruction

A

Obstruction of the normal movement of bowel contents – mechanical blockage of the bowel due to structural pathology

Classification:

  • Small or Large bowel
  • Partial or Complete obstruction
  • Simple or Strangulated
50
Q

State some common causes of small bowel obstruction

A
  • Previous surgery forming intra-abdominal adhesions
  • Incarcerated inguinal hernia
  • Crohn’s disease
  • Intestinal malignancy
  • Appendicitis
51
Q

State some common causes of large bowel obstruction

A
  • Colorectal adenomas/polyps
  • Malignancy- colorectal cancer
  • IBD
  • Diverticular disease
  • Volvulus
  • Previous abdominal surgery
52
Q

Summarise the epidemiology of bowel obstruction

A

Intestinal obstruction is a common surgical emergency- 20% of admissions with acute abdominal pain.

Of these patients, around 20% will have large bowel obstruction.

53
Q

What are the presenting symptoms of intestinal obstruction?

A
  • intermittent severe cramping pain
    • continuous pain = bowel ischaemia
  • abdominal distension + guarding
    • generalised tenderness
    • localised suggests perforation over that area
  • N+V
    • more common in small bowel obstruction
  • complete constipation and failure to pass flatus
    • tenesmus
  • peritonitis
    • ​secondary to perforation
    • rigidity
  • Tympanic abdomen
    • air in bowel
  • pyrexia, tachycardia
    • suggests ischaemia, strangulation, or an obstructed hernia causing systemic response
54
Q

Compare the appearances of a small bowel and large bowel obstructions

A

SBO

  • Dilated bowel obstruction >3cm
  • CENTRAL gas shadows
  • valvulae conniventes that completely cross the lumen

LBO

  • dilated bowel >6cm-9cm
  • PERIPHERAL gas shadows proximal to blockage
  • haustra do not cross whole lumen width
55
Q

What investigations would you order for a suspected bowel obstruction?

A

Bloods

  • FBC- neutrophilia in perforation, anaemia in CRC
  • U+Es- hypokalaemia due to fluid loss/vomiting
  • CRP
  • ABG- elevated lactate indicates extent of ischaemia. lactic acidosis may indicate perforation or necrosis

Imaging

  • CT abdo pelvis with contrast
    • identify the level and cause of the obstruction
    • tumour, hernia, volvulus, or gallstone, adhesions
  • AXR
  • Water soluble contrast enema- if fail to improve in 48hrs
    • xray w contrast
56
Q

How is obstruction managed?

A

Strangulation and large bowel obstruction require urgent surgery.

Ileus and incomplete small bowel obstruction can be managed conservatively, at least initially.

  • Emergency laparotomy in acute obstruction
  • NBM, insert NG tube
  • Gastric aspiration via NG tube if the patient is vomiting
  • IV fluids to rehydrate
  • Electrolyte replacement
  • Analgesia
  • Urinary catheter and fluid balance
  • Monitor vital signs, fluid balance and urine output
57
Q

Identify possible complications of intestinal obstruction

A

Medical emergency- good prognosis if treated quickly.

In untreated patients, obstruction progresses to intestinal necrosis, perforation, sepsis, and multi-organ failure.

Underlying cause of obstruction determines prognosis

58
Q

Define peritonitis

A

Inflammation of the peritoneal lining of the abdominal cavity.

It can be localised to one part of the peritoneum or generalised.

59
Q

State the causes of localised + generalised peritonitis

A

LOCALISED

  • Appendicitis
  • Cholecystitis
  • Diverticulitis
  • Intestinal obstruction

GENERALISED

  • Spontaneous bacterial peritonitis
    • patients with ascites, nephrotic syndrome
  • Secondary generalised peritonitis
    • bacterial translocation from a localised focus
    • eg from perforation

Localised and secondary generalised peritonitis is COMMON in surgical patients

60
Q

What are the symptoms of peritonitis?

A

Abdominal pain- continuous, sharp, localised, exacerbated by movement and coughing

Fever and abdominal pain are the two most common presenting symptoms.

Others include:

  • nausea, vomiting
  • haematemesis
  • haematochezia
  • melaena
61
Q

What are the signs of peritonitis on physical examination?

A

Localised Peritonitis

  • Tenderness on examination
  • Guarding
  • Rebound tenderness

Generalised Peritonitis

  • Very unwell
  • Systemic signs of toxaemia or sepsis (e.g. fever, tachycardia)
  • The patient will lie still
  • Shallow breathing
  • Rigid abdomen
  • Generalised abdominal rebound tenderness
  • Reduced bowel sounds (may be absent due to paralytic ileus)
62
Q

Identify appropriate investigations for peritonitis

A

Bloods

  • FBC- leukocytosis, anaemia
  • U+Es- creatine high in hepatorenal syndrome
  • LFTs- signs of liver disease
  • Blood cultures
  • Amylase – acute pancreatitis causes similar signs so check amylase!!

Imaging- checking for signs of seconary peritonitis

  • Erect CXR (check for air under the diaphragm)
  • AXR (check for bowel obstruction)
  • USS or CT abdomen

If Ascites

  • Ascitic tap and cell count
  • Neutrophils >250 cells/mm³ = SBP
  • Ascitic gram stain and culture
63
Q

How is peritonitis managed?

A

Localised peritonitis- treat cause

Generalised peritonitis

  • IV fluids
  • IV antibiotics
  • Urinary catheter, central venous line (to monitor fluid balance)
  • NG tube
  • IV Albumin for SBP
  • Laparotomy- remove the infected or necrotic tissue
  • Peritoneal lavage (large volume paracentesis)
64
Q

Identify possible complications of peritonitis

A

Early

  • Septic shock
  • Respiratory failure
  • Multiorgan failure
  • Paralytic ileus
  • Wound infection
  • Abscesses

Late

  • Incisional hernia
  • Adhesions
65
Q

Summarise the prognosis for patients with peritonitis

A
  • Localised: resolves with treatment of underlying cause
  • Generalised: higher mortality (30-50%)
  • Primary peritonitis: good prognosis with Abx treatment
  • SBP: mortality > 30% if diagnosis and treatment is delayed
66
Q

Define Pilonidal sinus

A

Disease where hair follicles become inserted into the skin of the natal cleft, creating a chronic sinus tract in the sacrococcgeal area

67
Q

Explain the pathogenesis of a pilonidal sinus

A
  1. Broken hair is driven into the skin of the natal cleft by a rolling action of the buttocks.
  2. This provokes a foreign body-type reaction, and chronic inflammation results in a mature sinus.
  3. Sinuses may be multiple and communicate via a deep cavity.
  4. Chronic discharge usually occurs.
  5. Infection may supervene and lead to an abscess.
68
Q

What are the risk factors for pilonidal sinuses?

A
  • Male sex (greater hirsutism)
  • age 16-40- due to hair charactersitics
  • Stiff hair
  • Hirsutism
  • Spending a long time sitting down
  • Obesity
69
Q

What are the presenting symptoms of pilonidal sinus?

A
  • Sacrococcygeal swelling, pain + discharge +/- sinues tracts
  • Skin maceration- due to chronic irritation of discharge
  • Abscess if superinfection occured

Fever or toxaemia- complication of abscess

Often recurrent

70
Q

Identify appropriate investigations for pilonidal sinu

A

NONE needed- clinical diagnosis

  • Bloods - to check for signs of infection
  • Raised WCC
  • Fasting glucose (diabetics are at risk)
71
Q

Generate a management plan for pilonidal sinus

A

Consider pre-op antibiotics

  • Acute Pilonidal Abscess*
  • Incision and drainage
  • Chronic Pilonidal Sinus*
  • Excision under general anaesthesia with exploration

Prevention

  • Good hygiene
  • Shaving
72
Q

Identify possible complications of pilonidal sinus

A
  • Pain
  • Infection
  • Abscess
  • Recurrence
73
Q

ummarise the prognosis for patients with pilonidal sinus

A
  • Good with drainage
  • Shaving will cure in most cases
  • Usually resolves by the age of 40
74
Q

Define alcohol withdrawal

A

Syndrome caused by abstinence from alcohol in a person with alcohol dependence.

Symptoms typically begin 6-12 hours after the patient’s last alcoholic drink

May progress to life-threatening delirium tremens, with or without seizures.

75
Q

Explain the pathophysiology of alcohol withdrawal

A

Alcohol interacts with 2 main receptors in the CNS:

  • Stimulates:*
  • inhibitory GABA receptors ⇒ downregulation
  • Inhibits:*
  • ​excitatory NMDA (glutamate) receptors ⇒ upregulation

Chronic alcohol also stimulates excitatory glutamate release, whilst inhibiting reuptake.

Excessive glutamatergic stimulation with decreased GABA activity leads to clinical symptoms of withdrawal

76
Q

Summarise the epidemiology of alcohol withdrawal

A

High global prevalence of harmful drinking

If untreated, 6% of alcohol-dependent patients develop clinically relevant symptoms of withdrawal

77
Q

Summarise the prevalence of alcohol withdrawal symptoms in dependent people

A

25% AW patients experience hallucinations

10% seizures

5% progress to delerium tremens

78
Q

What are the risk factors for alocohl withdrawal syndrome (AWS)?

A
  • Prior AWS and delirium tremens- frequent recurrence
  • Abrupt alcohol withdrawal in a dependent patient
79
Q

What are the mild presenting symptoms of AWS?

A

PRESENT 6-12 HOURS AFTER LAST DRINK

  • Psychiatric disturbance
    • Anxiety/restlessness
    • agitation is a sign of more severe withdrawal
  • Insomnia, fatigue
  • Headache
  • Signs of autonomic dysfunction:
    • tachycardia (more severe)
    • sweating
    • tremor (ask PT to extend hands. mild if you can feel but not see, severe if you can see without arms extended)
    • plapitations
  • Anorexia, N+V (don’t forget acute pancreatitis)
  • Alcohol cravings
  • Depression
80
Q

What are the severe presenting symptoms of AWS?

A

THESE PRESENT 12-48 HOURS AFTER LAST DRINK

(in order of severity)

  1. Hypertension, fever
  2. Hallucinations/psychiatric disturbances
  3. Seizures- generalised tonic-clonic
    • may be the first manifestation of alcohol withdrawal
    • most common cause of status epilepticus
    • don’t forget other causes (drugs, hepatic dysfunction)
  4. Delerium Tremens
    • medical emergency, high mortality
81
Q

What is the most severe outcome/symptom of alcohol withdrawal?

A

Delerium Tremens

Tends to appear 48-72 hours after last drink

Rapid onset confusion with difficult to control symptoms:

  • Profound confusion/delirium
  • Visual, auditory and tactile hallucinations
    • characteristically frightening
    • hyperalert state, respoonding to unseen stimuli
    • tactile- ‘insects crawling under skin’, pins+needles
  • Coarse tremor
  • Clinical instability:
    • Tachycardia
    • fever
    • circulatory collapse
    • ketoacidosis
    • increases risk of mortality
82
Q

What blood investigations would you do for suspected AWS?

A
  1. VBG
    • Respiratory alkalosis with hyperventilation
    • Metabolic acidosis with vomiting / alcoholic ketoacidosis (low vs high anion gap)
  2. BM
    • hypoglycaemia 2/2 poor nutrition, heavy alcohol use
  3. FBC
    • high MCV- in chronic alcoholics due to B12/thiamine deficiency
    • thrombocytopaenia-
      • toxicity of alcohol on platelet survival/function/production
      • folate deficiency
      • splenomegaly
  4. U+Es
    • electrolyte deficiencies (hypo- magnesaemia, phosphataemia, kalaemia)
    • can cause arrhythmias- ECG!!
  5. LFTs
    • Classic ratio of AST:ALT >2 in alcoholics
    • ie ALT higher than AST
    • GGT >10x ULON commonly associated with excessive drinking (
  6. Clotting screen
    • prolonged INR and PT in chronic liver disease
83
Q

How is AWS managed?

A
  • Supportive care
    • low lighting, minimal stimulation
    • ensure adequate fluids, correct electrolyte imbalances
    • oral/IV glucose
  • Treat any acute illness caused by alcohol- commonly associated with:
    • pneumonia/gastritis/hepatitis/pancreatitis
  • Benzodiazepines 1st line
    • Lorazepan for delerium tremens/seizures
      • short acting
    • Chlorediazepoxide/diazepan
      • ​long acting (less acute AWS)
  • Anticonvulsants if necessary
    • carbemazepine/clomethiazole may also be used
  • Thiamine (Pabrinex)
    • to prevent Wernicke’s encephalopathy
84
Q

Identify possible complications/prognosis of alcohol withdrawal

A

Patients can have seizures + die if untreated

Delirium tremens has a mortality of 35% if untreated

Mortality is < 2% with early detection and treatment

85
Q
A

YR3 Gastro (12 decks)

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