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Priapism.ppt sumit

quick guide to priapism..

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Priapism.ppt sumit

  1. 1. Presenter – Dr. Sumit S. HadgaonkarModerator – Dr. Ak. Kaku Singh
  2. 2. Definition A pathological condition of penile erectioncharacterized as prolonged and devoid of sexualstimulation or excitement. Persistent painful purposeless (uncontrolled) erectionof the penis (or clitoris) > 4hours Corpora cavernosa only all age groups (including newborns) usually pain (except in non-ischaemic type)
  3. 3.  Priapos (Priapus) was theGreek God of fertility who isusually pictured with amassive erection. This painting wasdiscovered in the wall of atemple in Pompeii, destroyedby the eruption of MountVesuvius in 79 AD. It showsPriapos “weighing his erection.”
  4. 4. Epidemology Occurrence although deemed infrequent ismeasurable Internationally: no information available Intracaverous injection therapy led to rise in no. ofcases Sickle cell disease (SCD) most common cause inpediatric age group 29 % - 45 % life time probability for SCD fordevelopment of priapism
  5. 5. Demographics Race - no predilection (although sickle cell disease, ofcourse, is a condition of the African Americanpopulation) Sex - disease of males. Clitoral priapism has beendescribed rarely Age - all ages, but peak in sickle cell patients between19 & 21 years
  6. 6. Anatomy
  7. 7. Anatomy
  8. 8. Anatomy
  9. 9. Physiology Penile erection generated by sensory stimulation of genitalia spinal reflex arc - reflexogenic erection afferent from penis through pudendal nerve to sacral spinalerection center (S2-S3-S4) efferent parasympathetic fibers travel back in Nervi erigentesand stimulate blood vessels of corpora cavernosa sympathetic fibers in thoracolumbar erection center (T12-L1)innervate vas deferens
  10. 10. Physiology Penile erection generated by psychogenic stimuli from higher brain centers descend through lateralcolumns and stimulatethoracolumbar andsacral spinal erectioncenters
  11. 11. Physiology Nitric oxide - an endogenous vasodilator - is released fromnerve endings and endothelial cells and binds to receptors onsmooth muscle of corpora cavernosa Cyclic guanosine monophosphate (cGMP) is formed,relaxing smooth muscle and allowing engorgement Phosphodiesterase type 5 (PDE5) catalyzes cGMP to GMP,leading to reversal of the above process Sildenafil (Viagra®), a recently released drug for erectiledysfunction, acts as a PDE5 inhibitor, helping to maintain aphysiologic erection
  12. 12. Pathophysiology Persistent erection of corpora cavernosa due todisturbances in detumescence mechanisms - i.e.inflow >> outflow Corpora spongiosum of the glans and peri-urethralregion unaffected Arterial high-flow - usually due to rupture ofcavernous artery and unregulated flow into lacunarspaces - NOT generally painful Veno-occlusive (low-flow) - full and unremittingcorporeal veno-occlusion
  13. 13. Mortality and Morbidity Deaths have been reported in patients with sickle celldisease and priapism, but due to complications fromunderlying disease process Main morbidity is long-term impotence, especiallywhen diagnosis and treatment are delayed
  14. 14. Etiology Hematological dyscrasias1.SCD2.Other hemoglobinopathies3.Leukamia – Chr. Granulocytic variant4.asplenisa5.Fabry’s disease Thrombotic risk1.erythropetin use2.hemodialysis (even with heparin)3.cessation of oral warfarin4.TPN (containing 20% fat emulsion)
  15. 15. Contd.. Non hematological malignancies1. Ca penis, urethra ,bladder ,prostate, kidney2.rectosigmoid carcinoma Neurological conditions1.lumbar disk prolapse2.spinal cord injury3.lumbar canal stenosis4.cauda equina compression from metastases5.anaesthesia – both GA and SA
  16. 16. Contd… Trauma ( presentation is delayed)1. direct penile or perineal trauma2.traumatic needle insertion for intracavernousinjection Erectile dysfunction therapy1. Intracavernous injections2.intra urethral alprostadil3.sildenafil
  17. 17. Contd.. Other drugs1.Antihypertensives – hydralazine ,alpha blockers2.antipsychotics and antidepressants – SSRIs,phenothiazines etc.3.Heavy alcohol intake4. Immunosuppressants - tacrolimus5.Androgen supplements6. Scorpion toxins Idiopathic – account for 50% off the total cases
  18. 18. SCD
  19. 19. CLL
  20. 20. Caverject® self-injectionUrethralsuppository
  21. 21. Vacuum pumps andother “sexual aids”
  22. 22. Phoneutria nigriventer - "armed spider"
  23. 23. Priapism caused by Phoneutria bite
  24. 24. Classification Low flow or Ischaemic (veno-occlusive) most common Painful sec to tissue ischemia and smooth musclehypoxia (compartment syndrome) Nonischaemic (arterial) less common up regulated cavernous inflow usually not fully erect and painless
  25. 25. Low-flow priapism Low flow or Ischemic (veno-occlusive) most common Penis fully erect (sludging of blood within) Painful sec to tissue ischemia and smooth musclehypoxia (compartment syndrome) blood gases from corpora – acidosis,hypoxia,hypercapnia NO & prostacyclin platelet aggregation and adhesion - thrombus formationand tissue damage Increased risk of fibrosis, irreversible cavernous tissuedamage and erectile function loss Causes ---most off them earlier noted Emergency management required
  26. 26. High-flow priapism Nonischaemic (arterial) less common Penile, perineal or pelvic trauma uncontrolled arterial inflow directly into the penilesinusoidal spaces usually penis not fully erect and painless often prolonged history normal local blood gases no risk of ischemia and subsequent fibrosis
  27. 27. Fractured penis
  28. 28. Priapism variants Stuttering priapism-recurring episodes-associated with SCD- every episode same as low flow or ischemic Refractory priapism-non ischemic priapism after treatment for ischemicvariety Neurogenic priapism-defect in neuroregulation of erection-it may be central or periphera Drug induced-both ischemic and non ischemic type of priapismproduced
  29. 29. Diagnosis History and physical examination-history should address pain ,duration, prior episodes,prior clinical treatment ,erectile status prior to attack-inspection and palpation of penis and abdomen.- involvement of all 3 structures i.e. glans ,spongiosm, cavernosa
  30. 30. Lab work up CBC – for hematological abnormalities Retic count and electrophoresis – for SCD and otherhemoglobinopathies Urine toxicology – for psychoactive drug abuse Other routine investigations
  31. 31. Penile diagnostics Aspirate from cavernosum tested for ABG Color Duplex ultrasound – can be used as analternative to aspiration and ABG Ultrasound – should be done in lithotomy positionand should start with perineum first and then entirepenile shaft- can diagnose anatomical abnormalitiesassociated with non ischemic variety Penile arteriography- mainly used for therapeuticpurpose
  32. 32. Treatment Differ according to type Based on diagnostic findings Stepwise approch applied based on1.reversibility2. invasiveness Treatment of historical interest1.medical -hot water bath 2. surgical-- ice packs -penile nerve-enemas transaction- sedatives -dorsal artery- leeches ligation
  33. 33. Treatment of Ischemic Priapism Aspiration of cavernous blood Treatment of related systemic condition Surgical treatment Penile prosthesis
  34. 34. Aspiration of cavernous blood Decompression by aspirating cavernous blood with orwithout saline irrigation – first line treatment Scalp vein needle 19-21 G directly inserted intocavernosum Saline irrigation with intracavernous phenylephrineimproves results Done after dorsal penile or penile shaft block Transglanular intracavernous needle insertion better thanlaterally placed needle
  35. 35. Treatment of related systemiccondition For those priapism associated with known systemiccausee.g. Priapism in SCD patients should be managed inline of sickle cell crisis by hydration, oxygenation,alkalinization,analgesia.
  36. 36. Surgical treatment For priapism beyond 48-72 hrs Surgical shunt – to drain blood from cavernosa bypassingveno-occlusive mechanism Shunts –1.Distal cavernoglanular shunts–a) Winter shunt : large biopsy needle through glans tocavernosab)Ebbehoj shunt : scalpel though glans to cavernosac) El –Ghorab shunt :excision of tunica albugenia at tipof cavernosum
  37. 37.  Proximal shunts –a)Quackels / Sacher Shunt : creation of windowbetween cavernosum and spongiosumb) Grayhack shunt : saphenous vein anastomosed withone of the cavernosa Shunts close after some time hence no permanenterectile dysfunction (ED) noted . Shunt complications : 1.urethral fistula2.purulent cavernositis3.pulm. embolism (Grayhack)
  38. 38. Penile prosthesis Significantly delayed presentations that predictablyresulting in erectile dysfunction Early prosthesis placement recommended Fibrosis complicates treatment on a later date
  39. 39. Treatment of non-ischemicpriapism Observation –spontaneous resolution in 62% cases- even duration even in years dose notaffect the outcome Selective arterial embolisation – for patients desirousof immediate solution- both permanent and temporary materials canbe used- temporary used (for ED prevention) Exploration and direct surgical ligation of sinusoidalfistulas or pseudoaneurysms-50% ED rate
  40. 40. Treatment of Stuttering priapism Treatment of all episodes in line of ischemic priapism Preventive strategy :1.Hormonal agents- most efficacy2.self injection of phenylephrine3.baclofen4.digoxin5.terbutaline
  41. 41. Miscellaneous medical treatment Hydroxyurea – for SCD TPA/ streptokinase – for ischemic Methylene blue – for high flow priapism
  42. 42. Priapism - complications Impotence: about 50% incidence Younger patients seem to do better Fibrosis: related to tissue ischemia Makes prosthesis placement difficult Gangrene: due to ischemia and infection Suprapubic catheter may help avoid
  43. 43. Fournier’s gangrene
  44. 44. THANKYOU

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