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Sickle-cell anemia
Section
of
the
Federal dental services Sickle-cell anemia A case
of
dental
interesi
Hobert Louis Xassucco, Captain,
1’9dE’
(DC)*
S
ickle-cell anemia, a hereditary, familial, chronic form of anemia, is a disease whose manifestations should be understood by the oral surgeon and the general practitioner prior to and during the treatment of dental infection, particularly if general anesthesia is to be used. In this article an attempt will be made to interrelate the characteristics of this disease v&h the oral surgical, ge’neral anesthetic, and roentgenographic aspects of dentistry. The sickle-cell trait occurs predominantly in Negroes and is found in approximately 8.5 per cent of the Negro population of the United States. True sickle-cell anemia is found in only 0.3 to 1.3 per cent of this gr0up.l When the gene for sickling is heterozygous, the patient will have the sickle trait or hemoglobin SA. When this gene is homozygous, one will find true sickle-cell anemia or hemoglobin SS. Persons with the sickle-cell trait may lead normal lives, but few with the true anemia live beyond the age of 30 years. Clinically, the patient may present the following symptoms: (1) fatigue and weakness; (2) pains in the long bones and joints; (3) pains of the “hand and foot syndrome.“’ (4) cardiomegaly and systolic murmurs characteristic of many anemias; (5) chronic leg ulcers, particularly over t,hc internal and external maleoli; (6) severe abdominal pain, especially in sickling crises; (7) occasional episodes of epistaxis; (8) icteric sclerac; (9) bone deformitics, such as a towershaped skull, kyphosis, and scoliosis; (10) pallor of the oral mucosal surfaces, particularly the palatine and buccal areas. Splenomegaly and hepatomegaly are rarely encountered. Laboratory studies of these patients reveal the picture of sickle-cell disease. The erythrocyte count may be between l,OOO,OOOand 2,000,OOO.The hemoglobin and hcmatocrit arc low. Leukocytosis is almost invariably present, probably because of the increa.sed hematopoietic activity. The differential white blood count is usually within the normal range. There is a decreased sedimentation rate, which is probably due to abnormal linkages formed by sickled cells which prevent formation of rou1eaux.l The platelet count is elcvatcd, and the bleeding and *Present
address:
Rox 2435, Ernest
Harmon
Air
Force Base, Stephenville,
Newfoundland.
397
398
Ma~ssucco
O.S., O.M. & 0.1’. hIarch, 1966
clotting times are normal. The reticulocyte count may be elevated, and this also is caused by increased hematopoietic activity and failure of the cells to reach maturation. A test for sickle cells may be performed by adding one drop of the reducing agent, sodium metabisulfitc, to a blood smear, thus reducing the ox>-gen tension and causing the cells to sickle.’ The roentgenographic appearance is interesting from the standpoint of boric chanigcs. Osteoporotic lesions may bc seen in some casts as a result of the erythroblastic hyperplasia of the marrow spaces, causing resorption of the medullary bone and thinnin, 17 of the cortical layer.:‘-” These changes arc VW! definitely seen in dental films. Other regions in which they are seen include the femur, tibia, fibula, sternum, and skull. In a study by Robinson and Sarnat” of twenty-two patients with sickle-cell anemia, dental roentgenograms showed dcfinite generalized osteoporotic changrs in cightccn cases. In this same study only the patients revealed extcnsivc osteoporosis in Ion,rr hones, eight had moderate changes, seven were mildly involved, and four had no traces. Lateral skull films may show a “hair-on-end” appearance which is produced by trabecular striations which radiate outwardly perpendicular to the inner table.’ The pattern of trabeculation seen in the dental film is perhaps more definitive because a smaller area is more closely examined and there is less tissue between the film and the bone.” These t,rabeculations may have a “stepladder” effect,” or thry may be entirely absent, as will be shown in the case to bc presented. These characteristics may bc well demonstrated in the most active hematopoietic region of the maxillae, namely, thn posterior region of the body of the mandible. Sickle-cell anemia may be first diagnosed when parent,s bring a child to the emergency ward of the hospital in a state of “crisis. ” This is usuallp characterized by cpistaxis, severe abdominal pain to the point of prostration, elevated tempcraturc, complaints of joint and long-bone pain, nausea, and vomiting. It is obvious from these symptoms that t,his illness could mimic a great number of other conditions, such as rheumatic fever, perforated ulcer, intestinal obstruction, or a ruptured spleen which would rcquirc surgical intervention.’ The following case report is presented to illustrate the classic patterns of sickle-cell anemia and its relationship to treatment h>- the dental surgeon. CASE REPORT IL M., a i-year-old Negro girl, was admitted to Worcester City Hospital, Worcestw, Massachusetts, in a “sickle-cell crisis” which was not diagnosed at the time. With a history of vomiting bloody material, a hemoglobin of 4.4 Gm., a hcmatocrit of 14 per cent, and a temperature of 100” F., the child was admitted for work-up and further study. The significant laboratory findings were as follows: Hemoglobin-8.6 Gm. (after transfusion) Hematocrit-25 per cent (after transfusion) White blood count-15,200 Platelets-530,000 Reticulocytes-2.5 per cent, 5.7 per cent, 6 per cent 2 days Sickle-cell preparation-Positive (sodium metabisulfite method) Blood smear-Marked anisoeytosis and poikiloeytosis In addition, a Grade 3 systolic precordial hemic murmur was discovered. Chest roentgenograms were normal but showed minimal rardiomegaly. The hemoglobin composition by electro-
Volume Kumber
21 3
Sickle-cell
memia
399
phoresis was type Sh, but this was later shown to be because of the transfusion. The hemoglobin determination was repeated and the results then showed type SS or true sickle-cell anemia. In addition to the Cckle-cell anemia, the child was found to have a urinary tract infection (culture showed colonies of Proteus mirabilis) and an alveolar abscess. Upon closer examination of the oral cavity, the mucosa appeared quite pale, especially that of the palate and the cheek. The tongue was also pale. The gingiva, although mildly d pea-sized swelling, which had pointed, was noted pale, showed no periodontal infection. on the buccal side of the left deciduous first molar. This tooth was extremely sensitive to percussion. The right and left deciduous molars were carious also, lmt it was, decided that they should be restored and only the infected molar removed. At this time a behavioral problem prevented dental or lateral jaw films. However, the tooth was removed, vvit,h the for patient under restraints and local anesthesia. The patient was treated with antibiotics this and the urinary tract infection. She recovrred from the dental procedure, the urinary tract was effectively treated, and the crisis was resolved. The hemoglobin and hrmatocrit stabilized at 9.2 Gm. and 28 per cent, rcxpectirely, and the patient was discharged to be followed in the outpatient department. Two things should be noted at this point: (1) the effect of septicemia and (2) increased body temperature in a person with the true anemia, The two areas of infection were perhaps enough to precipitate the crisis. After treating this patient, the pediatric service decided to stutly the whole family ant1 the family tree shown in Fig. 1 was evolved. B. M. and one of her siblings, 112. M., were both found to have true sickle-cell anemia. Hemoglobin elentrophoresis studies confirmed these findings. Both parents were found to have hemoglobin SA, or the gene which is heterozygous and produces the sickle-cell trait. One other sibling was found to be lretwozygous and shelved the trait. Two other siblings were found to be normal. Tn May, 1964, M. M. anil R. M. mere referred to the out,patient dental clinic at the hospital by their school dentist, who thought that the carious teeth were too severely damaged to be restored. In view of the behavioral problem, it was decided to admit the children to the hospital and remove these teeth under light general anesthesia. The right and left mandibular molar regions (Fig. 2, E and F) showed complete lack of trabeculation, indicating perhaps areas of hyperplastic erythropoiesis. The lamina dura and the Mother
Father
a
B.M.
0 0
Pig. 1. Family
M.M.
Heterozygous
NCWTl2.1
Homozygous
tree of Patient
- l!rue
B. M.
Sickle
Anemia
- Sickle Trait Hgb SA
- Hgb
SS
-
Fig. 2. Dental roentgenogrems of Pati(lnt II. M. A, masillary right molar region; A’, maxillary central incisor region; C, maxillary left molar region ; I), mandibular central incisors; E’, right molar region showing absence of traberulation; P, mandibular left molar mar ldibular G, mandibular right molar region in normal ‘?-yearregi on also showing lack of trabeculation; old Caucasian boy (note difference io hone pattwnsl.
Volume 21 Number 3
Sickle-cell
anemia
401
crestal bone appeared normal, Other cases similar to this have been reported, but in them there was some evidence of “stepladder” trabecu1ation.s Laboratory studies at the time the two girls were admitted to the hospital for dental surgery procedures rcvtxaled the following : Pntirnt
Hemoglobin Hematocrit White blood count Anisocytes ILypochromocytes Poikilocytes Sickle-cell trait
Y. Al.
x.9 28 per cent 11,900 3+ 1+ 1+ Positive
Patient 7.9
13. 21.
22 per cent 13,600 3 1+ 1+ Positive
The pediatric service considered the girls well adjusted to the environment and thought that they would tolerate light, rapid anesthesia for the extractions. In addition to the usual regimen of iron and multivitamin tablets, the patients were started on V-Cillin K, 200,000 units (1 teaspoon) four times daily for 5, days, one day prior to the procedure. On May 6, 1964, after premeditation with atropine sulfate, lhoo gr., the patients were anesthetized with oxygen, nitrous oxide, and Fluothane, and the carious teeth were removed. Following the extractions, the operative sites were packed with gauze. Bleeding was minimal, and the girls tolerated the procedure well. There mere no postoperative indications of a sickling crisis in either child. The follow-up blood studies indicated only that in Patient B. M. the hemoglobin dropped from 8.9 to 8.2, which was attributed to some postoperative bleeding and oozing. The children were discharged 2 days postoperatively, in satisfactory condition, to be followed in the outpatient department.
DISCUSSION
There are several important factors to be considered in these cases. Children with sickle-cell anemia are very susceptible to infection (because of their chronic anemia) which, by increasing their body temperature, may initiate a sickle crisis.l Dental infections should be avoided and guarded against. Osteomyelitis due to Staphylococcus aweus and Salmonella,l depending on the area, has been reported in a number of eases of sickle-cell anemia, further necessitating antibiotic coverage if alveolar bone is exposed. Decrease in blood pEI and reduction of oxygen tension canse the ergthrocytes to sickle. In disease as well as under general anesthesia, the oxygen blood level a.nd plI must he kept at a normal level. Small cha,nges, even within the 0, dissociation curve, have been known to produce a sickling crisis. Vnnecessary preoperative sedation was avoided to assure normal respiration prior to anesthesia and minimal depression of respiration upon recovery from anesthesia. Once again, antibiotics should be used routinely to ensure protection against bacteremia established by the extractions, not only to avoid septicemia but also to avoid further damage to the already overtaxed heart. Thus, with a.dequatc preventive measures, further provocation of true sickle-cell crises may be avoided. SUMMARY
A cast of true sickle-cell anemia found in two young Negro girls has been reviewed. The diagnostic features found in dental films have been described,
402
Massucco
OS., O.M. & O.P. March? 1966
and the role of dental disease in the aggravation cussed. their
I wish to thank cooperation.
the pediatric
and anesthesia
staffs
of this anemia has been disof the Worcester
City
Hospital for
REFERENCES
1. Wintrobe, Maxwell M.: Hematology, ed. 5, Philadelphia, 1961, Lea & Febiger, chap. 13, pp. 674, 675, 681, 682, 689. 2. Burko, Henry, Watson, Janet, and Robinson, Margaret: IJnusual Bone Changes in Sickle Cell Disease in Childhood, Radiology 80: 957-962, 1963. 3. Goldberg, J. S. R., MacIver, d. E., and Went, L. N.: The Bone Changes in Sickle Cell Anemia and Its Genetic Variants, .J. Bone & *Joint Surg. 41-B: 711-718, 1959. 4. Rowe, C. W., and Hazzard, M. E.: Bone Defects in Sickle Cell Anemia, Radiology 68: 661, 195i. 5. Almklov, John R., Hansen, Arnold E., and Schneider, Martin: Long Bone Involvement in Sickle Cell Anemia, Pediatrics 3: 204-209, 1950. 6. Robinson, Irwin B., and Sarnat, Bernard G.: Roentgenographic Studies of the Maxilla and Mandible in Sickle-Cell Anemia, Radiology 58: 517-523,, 1952. 7. Campbell, E. H.: Acute Abdominal Pain in Sickle Cell Anemia, Arch. Surg, 31: 687, 1935. 8. Morris, Alan L., and Stahl, Sigmund 8.: Intraoral Roentgenographic Changes in Sickle-Cell Anemia, ORAL SURG., ORAL Mm. & ORAL PATH. 7: 788, 1954.
of
the
Federal dental services Sickle-cell anemia A case
of
dental
interesi
Hobert Louis Xassucco, Captain,
1’9dE’
(DC)*
S
ickle-cell anemia, a hereditary, familial, chronic form of anemia, is a disease whose manifestations should be understood by the oral surgeon and the general practitioner prior to and during the treatment of dental infection, particularly if general anesthesia is to be used. In this article an attempt will be made to interrelate the characteristics of this disease v&h the oral surgical, ge’neral anesthetic, and roentgenographic aspects of dentistry. The sickle-cell trait occurs predominantly in Negroes and is found in approximately 8.5 per cent of the Negro population of the United States. True sickle-cell anemia is found in only 0.3 to 1.3 per cent of this gr0up.l When the gene for sickling is heterozygous, the patient will have the sickle trait or hemoglobin SA. When this gene is homozygous, one will find true sickle-cell anemia or hemoglobin SS. Persons with the sickle-cell trait may lead normal lives, but few with the true anemia live beyond the age of 30 years. Clinically, the patient may present the following symptoms: (1) fatigue and weakness; (2) pains in the long bones and joints; (3) pains of the “hand and foot syndrome.“’ (4) cardiomegaly and systolic murmurs characteristic of many anemias; (5) chronic leg ulcers, particularly over t,hc internal and external maleoli; (6) severe abdominal pain, especially in sickling crises; (7) occasional episodes of epistaxis; (8) icteric sclerac; (9) bone deformitics, such as a towershaped skull, kyphosis, and scoliosis; (10) pallor of the oral mucosal surfaces, particularly the palatine and buccal areas. Splenomegaly and hepatomegaly are rarely encountered. Laboratory studies of these patients reveal the picture of sickle-cell disease. The erythrocyte count may be between l,OOO,OOOand 2,000,OOO.The hemoglobin and hcmatocrit arc low. Leukocytosis is almost invariably present, probably because of the increa.sed hematopoietic activity. The differential white blood count is usually within the normal range. There is a decreased sedimentation rate, which is probably due to abnormal linkages formed by sickled cells which prevent formation of rou1eaux.l The platelet count is elcvatcd, and the bleeding and *Present
address:
Rox 2435, Ernest
Harmon
Air
Force Base, Stephenville,
Newfoundland.
397
398
Ma~ssucco
O.S., O.M. & 0.1’. hIarch, 1966
clotting times are normal. The reticulocyte count may be elevated, and this also is caused by increased hematopoietic activity and failure of the cells to reach maturation. A test for sickle cells may be performed by adding one drop of the reducing agent, sodium metabisulfitc, to a blood smear, thus reducing the ox>-gen tension and causing the cells to sickle.’ The roentgenographic appearance is interesting from the standpoint of boric chanigcs. Osteoporotic lesions may bc seen in some casts as a result of the erythroblastic hyperplasia of the marrow spaces, causing resorption of the medullary bone and thinnin, 17 of the cortical layer.:‘-” These changes arc VW! definitely seen in dental films. Other regions in which they are seen include the femur, tibia, fibula, sternum, and skull. In a study by Robinson and Sarnat” of twenty-two patients with sickle-cell anemia, dental roentgenograms showed dcfinite generalized osteoporotic changrs in cightccn cases. In this same study only the patients revealed extcnsivc osteoporosis in Ion,rr hones, eight had moderate changes, seven were mildly involved, and four had no traces. Lateral skull films may show a “hair-on-end” appearance which is produced by trabecular striations which radiate outwardly perpendicular to the inner table.’ The pattern of trabeculation seen in the dental film is perhaps more definitive because a smaller area is more closely examined and there is less tissue between the film and the bone.” These t,rabeculations may have a “stepladder” effect,” or thry may be entirely absent, as will be shown in the case to bc presented. These characteristics may bc well demonstrated in the most active hematopoietic region of the maxillae, namely, thn posterior region of the body of the mandible. Sickle-cell anemia may be first diagnosed when parent,s bring a child to the emergency ward of the hospital in a state of “crisis. ” This is usuallp characterized by cpistaxis, severe abdominal pain to the point of prostration, elevated tempcraturc, complaints of joint and long-bone pain, nausea, and vomiting. It is obvious from these symptoms that t,his illness could mimic a great number of other conditions, such as rheumatic fever, perforated ulcer, intestinal obstruction, or a ruptured spleen which would rcquirc surgical intervention.’ The following case report is presented to illustrate the classic patterns of sickle-cell anemia and its relationship to treatment h>- the dental surgeon. CASE REPORT IL M., a i-year-old Negro girl, was admitted to Worcester City Hospital, Worcestw, Massachusetts, in a “sickle-cell crisis” which was not diagnosed at the time. With a history of vomiting bloody material, a hemoglobin of 4.4 Gm., a hcmatocrit of 14 per cent, and a temperature of 100” F., the child was admitted for work-up and further study. The significant laboratory findings were as follows: Hemoglobin-8.6 Gm. (after transfusion) Hematocrit-25 per cent (after transfusion) White blood count-15,200 Platelets-530,000 Reticulocytes-2.5 per cent, 5.7 per cent, 6 per cent 2 days Sickle-cell preparation-Positive (sodium metabisulfite method) Blood smear-Marked anisoeytosis and poikiloeytosis In addition, a Grade 3 systolic precordial hemic murmur was discovered. Chest roentgenograms were normal but showed minimal rardiomegaly. The hemoglobin composition by electro-
Volume Kumber
21 3
Sickle-cell
memia
399
phoresis was type Sh, but this was later shown to be because of the transfusion. The hemoglobin determination was repeated and the results then showed type SS or true sickle-cell anemia. In addition to the Cckle-cell anemia, the child was found to have a urinary tract infection (culture showed colonies of Proteus mirabilis) and an alveolar abscess. Upon closer examination of the oral cavity, the mucosa appeared quite pale, especially that of the palate and the cheek. The tongue was also pale. The gingiva, although mildly d pea-sized swelling, which had pointed, was noted pale, showed no periodontal infection. on the buccal side of the left deciduous first molar. This tooth was extremely sensitive to percussion. The right and left deciduous molars were carious also, lmt it was, decided that they should be restored and only the infected molar removed. At this time a behavioral problem prevented dental or lateral jaw films. However, the tooth was removed, vvit,h the for patient under restraints and local anesthesia. The patient was treated with antibiotics this and the urinary tract infection. She recovrred from the dental procedure, the urinary tract was effectively treated, and the crisis was resolved. The hemoglobin and hrmatocrit stabilized at 9.2 Gm. and 28 per cent, rcxpectirely, and the patient was discharged to be followed in the outpatient department. Two things should be noted at this point: (1) the effect of septicemia and (2) increased body temperature in a person with the true anemia, The two areas of infection were perhaps enough to precipitate the crisis. After treating this patient, the pediatric service decided to stutly the whole family ant1 the family tree shown in Fig. 1 was evolved. B. M. and one of her siblings, 112. M., were both found to have true sickle-cell anemia. Hemoglobin elentrophoresis studies confirmed these findings. Both parents were found to have hemoglobin SA, or the gene which is heterozygous and produces the sickle-cell trait. One other sibling was found to be lretwozygous and shelved the trait. Two other siblings were found to be normal. Tn May, 1964, M. M. anil R. M. mere referred to the out,patient dental clinic at the hospital by their school dentist, who thought that the carious teeth were too severely damaged to be restored. In view of the behavioral problem, it was decided to admit the children to the hospital and remove these teeth under light general anesthesia. The right and left mandibular molar regions (Fig. 2, E and F) showed complete lack of trabeculation, indicating perhaps areas of hyperplastic erythropoiesis. The lamina dura and the Mother
Father
a
B.M.
0 0
Pig. 1. Family
M.M.
Heterozygous
NCWTl2.1
Homozygous
tree of Patient
- l!rue
B. M.
Sickle
Anemia
- Sickle Trait Hgb SA
- Hgb
SS
-
Fig. 2. Dental roentgenogrems of Pati(lnt II. M. A, masillary right molar region; A’, maxillary central incisor region; C, maxillary left molar region ; I), mandibular central incisors; E’, right molar region showing absence of traberulation; P, mandibular left molar mar ldibular G, mandibular right molar region in normal ‘?-yearregi on also showing lack of trabeculation; old Caucasian boy (note difference io hone pattwnsl.
Volume 21 Number 3
Sickle-cell
anemia
401
crestal bone appeared normal, Other cases similar to this have been reported, but in them there was some evidence of “stepladder” trabecu1ation.s Laboratory studies at the time the two girls were admitted to the hospital for dental surgery procedures rcvtxaled the following : Pntirnt
Hemoglobin Hematocrit White blood count Anisocytes ILypochromocytes Poikilocytes Sickle-cell trait
Y. Al.
x.9 28 per cent 11,900 3+ 1+ 1+ Positive
Patient 7.9
13. 21.
22 per cent 13,600 3 1+ 1+ Positive
The pediatric service considered the girls well adjusted to the environment and thought that they would tolerate light, rapid anesthesia for the extractions. In addition to the usual regimen of iron and multivitamin tablets, the patients were started on V-Cillin K, 200,000 units (1 teaspoon) four times daily for 5, days, one day prior to the procedure. On May 6, 1964, after premeditation with atropine sulfate, lhoo gr., the patients were anesthetized with oxygen, nitrous oxide, and Fluothane, and the carious teeth were removed. Following the extractions, the operative sites were packed with gauze. Bleeding was minimal, and the girls tolerated the procedure well. There mere no postoperative indications of a sickling crisis in either child. The follow-up blood studies indicated only that in Patient B. M. the hemoglobin dropped from 8.9 to 8.2, which was attributed to some postoperative bleeding and oozing. The children were discharged 2 days postoperatively, in satisfactory condition, to be followed in the outpatient department.
DISCUSSION
There are several important factors to be considered in these cases. Children with sickle-cell anemia are very susceptible to infection (because of their chronic anemia) which, by increasing their body temperature, may initiate a sickle crisis.l Dental infections should be avoided and guarded against. Osteomyelitis due to Staphylococcus aweus and Salmonella,l depending on the area, has been reported in a number of eases of sickle-cell anemia, further necessitating antibiotic coverage if alveolar bone is exposed. Decrease in blood pEI and reduction of oxygen tension canse the ergthrocytes to sickle. In disease as well as under general anesthesia, the oxygen blood level a.nd plI must he kept at a normal level. Small cha,nges, even within the 0, dissociation curve, have been known to produce a sickling crisis. Vnnecessary preoperative sedation was avoided to assure normal respiration prior to anesthesia and minimal depression of respiration upon recovery from anesthesia. Once again, antibiotics should be used routinely to ensure protection against bacteremia established by the extractions, not only to avoid septicemia but also to avoid further damage to the already overtaxed heart. Thus, with a.dequatc preventive measures, further provocation of true sickle-cell crises may be avoided. SUMMARY
A cast of true sickle-cell anemia found in two young Negro girls has been reviewed. The diagnostic features found in dental films have been described,
402
Massucco
OS., O.M. & O.P. March? 1966
and the role of dental disease in the aggravation cussed. their
I wish to thank cooperation.
the pediatric
and anesthesia
staffs
of this anemia has been disof the Worcester
City
Hospital for
REFERENCES
1. Wintrobe, Maxwell M.: Hematology, ed. 5, Philadelphia, 1961, Lea & Febiger, chap. 13, pp. 674, 675, 681, 682, 689. 2. Burko, Henry, Watson, Janet, and Robinson, Margaret: IJnusual Bone Changes in Sickle Cell Disease in Childhood, Radiology 80: 957-962, 1963. 3. Goldberg, J. S. R., MacIver, d. E., and Went, L. N.: The Bone Changes in Sickle Cell Anemia and Its Genetic Variants, .J. Bone & *Joint Surg. 41-B: 711-718, 1959. 4. Rowe, C. W., and Hazzard, M. E.: Bone Defects in Sickle Cell Anemia, Radiology 68: 661, 195i. 5. Almklov, John R., Hansen, Arnold E., and Schneider, Martin: Long Bone Involvement in Sickle Cell Anemia, Pediatrics 3: 204-209, 1950. 6. Robinson, Irwin B., and Sarnat, Bernard G.: Roentgenographic Studies of the Maxilla and Mandible in Sickle-Cell Anemia, Radiology 58: 517-523,, 1952. 7. Campbell, E. H.: Acute Abdominal Pain in Sickle Cell Anemia, Arch. Surg, 31: 687, 1935. 8. Morris, Alan L., and Stahl, Sigmund 8.: Intraoral Roentgenographic Changes in Sickle-Cell Anemia, ORAL SURG., ORAL Mm. & ORAL PATH. 7: 788, 1954.