Document jgL2vq4DMZbZxrkVGjzr0kNb2

! 472 F. Li. SMITH, 2n d , T. K. RATHMELL AMD G. E. MAliCIL TABLE 1 Clinical signs and symptoms of phtmhisjn GUOtH* J OBOD? JJi GltOXJP X BT300ELTIVB EYIJiKNCB OV s u g u k s t iv k i:viar..\cn or epaoEaTiv'B e y id t ^t x o p INCIPlHN'r INTOXICATION AN'O JflEb'lNlTVi, APVANCKD, AND ACTfV 1 Li:a !> Aijsom'rzo.v INACTIVE OU AlUtXSTUD PLtiMUJ-'iM w iv h a c v c i: PUIMMBU M A NINi-'HX ATI0 N A ' General symptoms t Patient becomes Pallor ' Anemia easily flustered, Jaundice Inanition moody, restless and Slight lead line Lead line , excitable Arthralgia Arthralgia Slight inanition Jaundice General feeling of Fatigued easily Genera! weakness malaise Hypotension to Normal Hypertension Slight pyrexia \ Pain in chest Wrist drop 3/ Foot drop 1,,. Digestive system Persistent metallic tasto Slight anorexia Slight constipation Metallic taste Coated tongue Anorexia Constipation Slight abdominal colic Metallic taste Coated tongue Anorexia Marked constipation Paroxysmal colic Nausea and Kinesis Rigid abdomen lllood in stool Irritability Unco&perativenoss Nervous system Slight frontal headache Slight tremors to Parkin- soman Syndrome Slight ataxia Insomnia Palpitation Increased reflexes Increased irritability Rye grounds may show choking of optic discs Severe frontal hoft'Jnr Tremors Confusion Ataxia Insomnia Convulsions Fibrillary twitching* Neuritis Visual disturbance* Kncephalitis Hallucinations Coma Paralysis Cerebral palsy N36838 DUP050308550 FAULT IHA0N0SI8' OF PLUMBISM 473 cnovn ,.-fcr.7-Tivcr.vii:NCBor juiOJ:moK TAULU l~Concludr.d OUOUJ* II fltKJOI'HTXV); r,Vtr>HNOJ3 ov iNCiviwr in*t io ; A2f 1WJVJ5 Oil A Itllh^TliD M.ThM HJKM <mour in fWOnKrytivn k v u ik k c r cr jDKmair, a iiv a ::c k t >, a md a c t iv b J'LVMIMftM Ml111 ACUTM MANIKKRTATION9 Renal symptoms which fluctuate!! Trace of albumin and few L-tween normal f-.rnnuliu' casts in urine limits ami a very Lend which fluctuates be e!i(.;!it rise tween norma! limits and a positive rioo Toxic nephrosis Albuminuria Casts in urino Homatoporphyrmuria Hem atta in Positive but fluctuating lead findings K should be remembered that all of these symptoms will never t,,; found in any single ease and frequently a patient is presented fur observation or treatment whose past history to lead exposure would cause one to expect symptoms conforming to Groups II or III when only those of Group I can be demonstrated. Many lesions have been reported associated with the above vvmploms of lead poisoning by the previously named inves tigators, as well as Taylor and Schrara* and Vigdortehik10, the most common of which arc: Arteriosclerosis, ulcers of the stomach and intestine, contracted small intestine, tubular and chronic interstitial nephritis, hemorrhages and exudates of the retina, neuro-retinitis, chronic nephritis (particularly in children), malignant hypertensive nourorctinitis, hypertensive encepha lopathy, hypertonia, ncuronophagia in cerebral sections, essential hypertension. Carlson11 showed that the symptoms of chronic arsenic poisoning resemble those of plumbism, and Lanza11 concluded dial many cases of mild lead poisoning are diagnosed as chronic ., yendicitis and even as gall bladder disease, with all too frequent .-urgical intervention. We have known eases of mild lead poisoning to be confused with intracranial and cord tumors. It has been shown by the majority of these investigators that many workers continually exposed to lead fail to exhibit clinical evidence of plumbism. This individual variance in. susceptibility