What is hypothenar hammer syndrome?
What is the incidence adn risk factors?
Post traumatic digital ischaemia by thrombosis of
ulna artery in Guyon's canal
Males 9:1 Females
usually dominant hand- ring or little finger, thumb spared
risks: vibration tools, sports- baseball catchers/ golfers
What is the pathology of hypothenar hammer syndrome?
single or repetitive blunt impact to hypothenar eminence -> ulna artery thrombosis or aneursym
Hook of hmate acts an avil for thrombosis
Describe the course of the ulna artery as it exits Guyon's canal?
It branches into 2 - Superifical and Deep branch
its relationship to the hook of hamate- over distal 2cm, the artery is directly anterior to the hook of the hamate, covered by palmaris brevis, subcutaneous tissue and skin
what are the symptoms and signs of hypothenar hammer syndrome?
What test could you do confirm diagnosis?
pain over hypothenar eminence and ring finger
blanching, mottlying, ulceration
tenderness over hypothenar eminence
pulsatile mass if aneurysm present
Allen's test- positive if occulsion
What imaging is useful for diagnosis?
What is ths Differential diagnosis for this condition?
Doppler- first line
Angiogram Ct/MRI to confirm occulsion around hook of hamate
Raynaud's disease- where the thumb is involved not so in hypothenar Hammer syndrome
What is the treatment for Hypothenar hammer syndrome?
Non operative: lifestyle changes- smoking cessation, avoid recurrent trauma= 80% success
Operative= when ischaemis in multiple digits= >
Resection of thrombotic / aneurysmal segment +/- local sympathectomy
Raynaud's syndrome consists of 2 diseases, name them?
What is the difference between Raynaud's disease and phenomenon?
Phenomenon= vasospastic disease with a cause/ disease
Disease= vasospastic disease with no cause found
Can you describe the eipdemiology of raynaud's phenomena?
Describe its pathology and signs?
Path: Periodic digital ischemia induced by cold temperature or sympathetic stimuli including pain or emotional stress
Signs- triphasic colour change- white- blue -red
white= due to vasospam
blue to venous statsis
red- rebound hyperaemia
What are the condiiton assocaited with Raynaud's phenenoma?
Connective tissue disorders-
CREST Syndrome= calcinosis, Raynaud's, Eosphaygeal dysmolitiy, scleroderma, telangectasia
Neurovascular Compression- thoracic oulet syndrome
Are studies helpful in raynaud's phenomenon?
What is the TX?
Yes often abnormal blood chemistry, microangiology, angiography
Tx Non operative : treat underyling disease
Are studies helpful in Raynaud's disease?
How is it tx?
No- normal biochem etc, normal allen's test, as no underlying diseae is causeative
Tx; Non operative
lifestyle changes, avoid cold temperature, cessation smoking
medication- ca channel blockers, dipyridamole (Persantine),
Surgery- Sympathectomy if consx tx fail
What is Buerger's disease aka Thromboangitis obliterans?
A nonartherosclerotic, segmental inflammatory disease of small and medium vessels of hands and feet
What is the epidemiology of Buerger's disease?
What are the risk factors?
Common in smokers
Typically effects patients <45 yrs
Males 3: 1 female
Smoking and chewinf tobacco
What is the pathology of Buerger's disease?
Inflammation and clotting of the small vessels of hand and feet
Acute- thrombus including neutophils occlud vessel lumen sparing wall.
Subacute- organisaiton of the thrombus
Chronic- inflammation subsides- organised thrombus and fibrosis remains
What is the prognosis of Buerger's disease?
94% who quit smoking avoid amputation
43% chance of amputation within 8 years if smoking is continued
What are the signs and symptoms of Buerger's disease?
Intermittent claudication of feet and hands
Numbness/ tingling in extremities
Signs- ulceration,large erythermatous blood vessels, necrosis of digit tips
sensory findings 70% patients
Positive allen's test
What investigations are useful for Buerger's disease?
Arteriography- see corkscrew vessels (pic)
What is the tx for Buerger's disease?
Symptomatic treatment- avoid cold, daily aspirin,gentle exercise
Smoking cessation is the only treatment known to reduce the chances of amputation
Sympathectomy- controversial- cut nerves in pain area
Amputation- if gangrene/non healing ulces/ refractory pain
What is this?
What is it characterised by?
Extensive soft tissue damage associated with exposure to temperatures below freezing point
What is the pathology of frostbite?
Cellular- movement of water from intracellular to extracellular which leads to cell dehyration and cell death
Ice crystals form extracellularly when temp = 6-15 degrees Celsius
Sensory nerve defecit ouccurs around 10 degrees celsius
What is the prognosis of frostbite?
Worsened with alcohol/ intoxication
Contat skin with ice/ metal
elevated wind chill factor
How does a patient present with frostbite?
Are any investigations helpful?
Development of blisters 6-24 hr post warming
superifical lesions= clear
Haemorrhagic- deeper= normal painless
Bone scan at 3rd day post injury can give idea on severity
How would you tx a patient with Frostbite?
Initial resuscitation with warm IV fluids
Rewarming of the affected extremity
Wound care and topical antibiotics (prevent superficial infections)
Rewarming of body part
Perform in waterbath at a temperature of 40-44 degrees Celsius for 30 minutes.
This may require IV analgesia or even conscious sedation. Repetitive freeze-thaw cycles should be avoided
Topical aloe vera, extremity elevation and splinting white/clear blisters- require debridement
hemorrhagic blisters- should be drained, but left intact
IV tissue plasminogen activator if no evidence of blood flow.
When would surgery be required in frostbite?
1) Circumferential frostbite-> Immediate surgical escharotomy
2) Surgical debridement +/- amputation - once demarcating is complete - may take 1-3 months
What are the complications of frostbite in adults?
Vasopasic disease- Ca channel blockers or surgical sympathetectomy
Premature Growth plate closure
Joint laxity, short digits, degenerative disease- seen in patients >10 yrs with earlier disease.
What is Complex Regional pain syndrome aka Reflex Sympathetic Dystrophy?
When is this condition caused causalgia?
Sustained sympathetic activity in perpetuated reflex arc characterised by pain out of proportion to phsical examination findings
When a defined nerve is involved
What is the pathophysiology?
Trauma from an exageratted response to trauma- common poor outcome post crush injury ( foot)
How can CRPS be prevented?
Vitamin C 500 mg daily is an effective prophylactic agent in distal radius fractures treated with conservative management-
Vitamin C also has been shown to decrease the incidence of CRPS (type I) following foot and ankle surgery
Avoid tight dressings and immobilisation
Vitamin C is thought to reduce lipid peroxidation, scavenge free hydroxyl radicals, protect the capillary endothelium, and inhibit vascular permeability.
RCT by Zollinger in Lancet 1999- 115 adults with 119 fractures treated with conservative management. They found that RSD/CRPS occurred in four (7%) wrists in the vitamin C group (500mg daily for 50 days) and 14 (22%) in the placebo group.
2nd study by Zollinger in JBJS Br317 adult patients sustaining 328 distal radius fractures treated conservatively. They had allocated treatment groups to 200mg, 500mg, or 1500mg vitamin C dosages for 50 days. RSD/CRPS occurrence was 4.2% in the 200mg group, 1.8% in the 500mg group, and 1.7% in the 1500mg group and thus the 500mg dosage for 50 days was recommended at the conclusion of the study.
surgically - Cazanueve et al belgium Acta orthop 2002- evaluated 195 patients who underwent open reduction internal fixation of a distal radius fracture. The first 100 did not receive vitamin C postoperatively. The next 95 patients received oral vitamin C for 45 days beginning the first day after surgery. The patients who received vitamin C had 5 times less incidence (2% vs. 10%) of reflex sympathetic dystrophy.
What is the classification system for CRPS?
Lankford and Evans ( bonnie lankford had red hair- red hands)
1) Acute 0-3 months, Pain, swelling, warmth, redness, decreased ROM, hyperhidrosis - picture- Normal xrays but positive 3 phase bone scan
2) Sub- Acute, 3-12mo, Worse pain, cyanosis, dry skin, stiffness, skin atrophy. xray= Osteopenia
3) Chronic >12 mo, Dimished pain, fibrosis, glossy skin, joint contractures. xray- Extreme osteopenia
What is the international study for pain classification of CRPS?
Type 1- CRPS without demonstrated nerve lesion=Most common
Type 2= CRPS with nerve damage
What are the cardinal signs of CRPS?
What do you find on clinical examination of CRPS?
Trophic skin changes
Flamingo gait if knee involved
What investigations are useful in CRPS?
Xrays- define level of ostepenia
3 Phase bone scan-
Phase 1 ( 2 mins)= arteriogram
Phase 2 (5-10mins) cellulitis/synovial inflammation
phase 3 ( 2-3rs) bone images
phase 4- (24hrs) differentiates Osteomyelitis from adjacent cellulitis
RSD shows positive phase 3 not correlation to phase 1/2
What effects CRPS outcome?
Successful early diagnosis
What is the TX of CRPS?
Analgesia- refer to pain team early: NSAIDs, alpha blocking agents( phenozybenzamine), antidepressants, anticonvulsants,GABA agonists, Ca channel blockers. bisophonates for osteopenia.
Physical therapy- gentle stretchings ( type 1), tactile discrimination training, graded motor imagery,
Nerve stimulation- only for type 2 if one nerve effected can place on that nerve area
Chemical sympathectomy- when other consx tx fail
Sympathectomy- failed consx mx