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
2
Q
Explain the pathophysiology of amyloidosis
A
Misfolding of immunoglobulin light chains into amyloid configuration
Go from being soluble → insoluble
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
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
7
Q
Define appendicitis
A
acute inflammation of the vermiform appendix
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
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
10
Q
What are the bacteria most commonly present in appendicitis?
A
Bacteroides fragilis
E. Coli
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
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.
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
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
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
16
Q
How is appendicitis managed?
A
- Prompt appendicectomy
- laparoscopy - diagnostic and therapeutic advantages
- Antibiotics:
- Cefuroxime
- Metronidazole
- Supportive treatment
- analgesia- morphine sulfate, IV paracetamol
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
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.
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
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.
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
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)
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
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
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
26
Q
Summarise the epidemiology of inguinal hernias
A
COMMON
Peak age in adults: 55-85 yrs
9 x more common in MALES
27
Recognise the presenting symptoms of inguinal hernias
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
28
Recognise the signs of inguinal hernias on physical examination
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
29
How do you discerne between direct and indirect inguinal hernias
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
30
Identify appropriate investigations for inguinal hernias
**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
31
How are inguinal hernias mangement
**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
32
Identify possible complications of inguinal hernias
* **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
33
Summarise the prognosis for patients with inguinal hernias
Prognosis is excellent after surgical repair
Slowly enlarge if left alone
34
Define Femoral Hernia
Abdominal contents pass through weakness **femoral canal**, presenting as a mass in the **upper medial** thigh
35
What is the epidemiology of femoral hernias
* 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**
36
Explain the risk factors of femoral hernias
* **Female**
* **Increasing age**
* **Pregnancy** – higher incidence in multiparous compared to nulliparous
* **Increased intra-abdominal pressure** e.g. heavy lifting, chronic constipation
37
What are the presenting symptoms of femoral hernias?
Lump in groin, **inferior to inguinal ligament**
Usually asymptomatic at presentation
Around **30% present as an emergency** due to obstruction or strangulation
38
Define intestinal (mesenteric) ischaemia
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
What are the 3 main types of ischaemic bowel disease?
1. **acute mesenteric ischaemia**
2. **chronic mesenteric ischaemia** (mesenteric angina)
3. **chronic colonic ischaemia**- ischaemic colitis
40
Explain the aetiology/risk factors of **mesenteric ishcaemia**
* **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
Which areas of the bowel are most affected by hypoperfusion?
**Washershed areas**
## Footnote
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
Define ischaemic colitis
**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
What are the risk factors for mesenteric ischaemia?
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
Summarise the epidemiology of intestinal ischaemia
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
Recognise the presenting symptoms of intestinal ischaemia
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
State some general symptoms of intestinal ischaemia
* 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
Recognise the signs of intestinal ischaemia on physical examination
* 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
Identify appropriate investigations for intestinal ischaemia
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
Define and classify intestinal obstruction
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
State some common causes of small bowel obstruction
* **Previous surgery** forming intra-abdominal adhesions
* **Incarcerated inguinal hernia**
* **Crohn's disease**
* **Intestinal malignancy**
* **Appendicitis**
51
State some common causes of large bowel obstruction
* Colorectal adenomas/polyps
* Malignancy- colorectal cancer
* IBD
* Diverticular disease
* Volvulus
* Previous abdominal surgery
52
Summarise the epidemiology of bowel obstruction
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
What are the presenting symptoms of intestinal obstruction?
* **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
Compare the appearances of a small bowel and large bowel obstructions
_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
What investigations would you order for a suspected bowel obstruction?
_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
How is obstruction managed?
**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
Identify possible complications of intestinal obstruction
**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
Define peritonitis
**Inflammation of the peritoneal lining** of the abdominal cavity.
It can be localised to one part of the peritoneum or generalised.
59
State the causes of localised + generalised peritonitis
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
What are the symptoms of peritonitis?
**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
What are the signs of peritonitis on physical examination?
_Localised Peritonitis_
* **Tenderness** on examination
* **Guarding**
* **_Rebound_ tenderness**
_Generalised Peritonitis_
* Very **unwell**
* **Systemic sign**s 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
Identify appropriate investigations for peritonitis
_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
How is peritonitis managed?
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
Identify possible complications of peritonitis
Early
* **Septic shock**
* **Respiratory failure**
* **Multiorgan failure**
* **Paralytic ileus**
* **Wound infection**
* **Abscesses**
Late
* **Incisional hernia**
* **Adhesions**
65
Summarise the prognosis for patients with peritonitis
* **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
Define Pilonidal sinus
Disease where **hair follicles** become **inserted** into the skin of the **natal cleft**, creating a **chronic sinus tract** in the **sacrococcgeal** area
67
Explain the pathogenesis of a pilonidal sinus
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
What are the risk factors for pilonidal sinuses?
* **Male sex** (greater hirsutism)
* **age 16-40**- due to hair charactersitics
* **Stiff hair**
* **Hirsutism**
* Spending a long time **sitting down**
* **Obesity**
69
What are the presenting symptoms of pilonidal sinus?
* **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
Identify appropriate investigations for pilonidal sinu
NONE needed- clinical diagnosis
* Bloods - to check for signs of infection
* Raised WCC
* Fasting glucose (diabetics are at risk)
71
Generate a management plan for pilonidal sinus
Consider **pre-op antibiotics**
* Acute Pilonidal Abscess*
* **Incision** and **drainage**
* Chronic Pilonidal Sinus*
* **Excision** under **general anaesthesia with exploration**
Prevention
* Good hygiene
* Shaving
72
Identify possible complications of pilonidal sinus
* Pain
* Infection
* Abscess
* Recurrence
73
ummarise the prognosis for patients with pilonidal sinus
* Good with drainage
* Shaving will cure in most cases
* Usually resolves by the age of 40
74
Define alcohol withdrawal
Syndrome caused by abstinence from alcohol in a person with alcohol dependence.
## Footnote
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
Explain the pathophysiology of alcohol withdrawal
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
Summarise the epidemiology of alcohol withdrawal
**High global prevalence** of harmful drinking
If untreated, **6%** of alcohol-dependent patients develop clinically relevant symptoms of withdrawal
77
Summarise the prevalence of alcohol withdrawal symptoms in dependent people
25% AW patients experience **hallucinations**
10% **seizures**
5% progress to **delerium tremens**
78
What are the risk factors for alocohl withdrawal syndrome (AWS)?
* **Prior AWS** and delirium tremens- frequent recurrence
* **Abrupt alcohol withdrawal** in a dependent patient
79
What are the _mild_ presenting symptoms of AWS?
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
What are the severe presenting symptoms of AWS?
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
What is the most severe outcome/symptom of alcohol withdrawal?
**_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
What blood investigations would you do for suspected AWS?
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
How is AWS managed?
* **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
Identify possible complications/prognosis of alcohol withdrawal
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
